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This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/your-eye-pressure-may-look-fine-at-the-doctor-while-hidden-spikes-at-home-still-drive-glaucoma-progression Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Your Eye Pressure May Look Fine at the Doctor—While Hidden Spikes at Home Still Drive Glaucoma Progression Yes: a reassuring pressure reading in the clinic can miss pressure changes that happen during the rest of the day. A study published online on September 30, 2026, found that two new measures of pressure above a patient’s own target were associated with faster visual-field decline when calculated from home readings—but not from office readings. The result is important, but it does not prove that pressure spikes caused the damage, or that home monitoring prevents it. () The key idea is simple: glaucoma care may learn more from a pattern of pressure readings than from one reading at an appointment. But today’s home devices take occasional readings, not continuous measurements, and the study’s “pressure burden” measures are still early research tools. What the September 30, 2026 study found The study, “In-office and remote intraocular pressure metrics associated with visual field progression in treated open-angle glaucoma,” compared pressure measurements taken at home with measurements recorded during routine clinic care. It asked whether different ways of summarizing pressure were associated with how quickly visual-field test results changed over time. () Its most notable finding was that average pressure and maximum pressure were not significantly associated with visual-field decline in this sample—whether measured at home or in the clinic. However, two measures that considered pressure relative to each patient’s individual treatment target—average and total excess above that target—were associated with faster decline in home readings. That distinction matters. This was a retrospective association study, not a trial that assigned patients to home monitoring or showed that reducing pressure burden prevents progression. The study can identify a signal worth investigating; it cannot establish cause and effect. Reconstructing the study population and measurements The researchers reviewed records from 397 treated patients with 777 eyes at Johns Hopkins University and the University of Utah. The final analysis included 94 patients and 150 eyes after exclusions. Patients had used an iCare HOME rebound tonometer between October 2018 and September 2024. The analysis focused on patients with open-angle glaucoma and excluded several other glaucoma types, including angle-closure, traumatic, and uveitic glaucoma. () Who was included? For the full table, please open this article on visualfieldtest.com. The mean visual-field result indicates a wide spread of glaucoma severity, not one uniform stage. The paper does not report how many eyes fell into each stage, so the average cannot be used to reconstruct those percentages. () What treatment were patients receiving? All participants were treated for glaucoma, and the researchers restricted the clinical record data to periods when treatment was consistent with the home-measurement period. Most patients were using at least one pressure-lowering eye drop. Before the home-monitoring period, many eyes had also undergone procedures, including cataract surgery, selective laser trabeculoplasty, trabeculectomy, or micro-invasive glaucoma surgery. These procedure categories can overlap. () Each patient’s target pressure was set by the treating glaucoma specialist as part of routine care. The target was intended to reflect factors such as disease severity, structural damage, starting pressure, and the clinician’s judgment. The paper analyzed target-based measures in 142 eyes, but the accessible report does not give a cohort-wide average target pressure. In other words, it does not support a claim that the group’s mean target was a particular number. That missing average is important: a target is not a universal biological boundary. It is a clinical estimate that should be revisited if the eye continues to worsen. Glaucoma guidelines likewise describe target pressure as individual rather than one fixed number for everyone. () How much home and clinic monitoring was done? Patients were trained to use the iCare HOME and instructed to take readings at least four times during waking hours: from waking to 10 a.m., 10 a.m. to 2 p.m., 2 p.m. to 6 p.m., and 6 p.m. until sleep. Each included eye had at least seven days of home readings; readings beyond ten days were excluded from the analysis. Patients actually made a median of 4.9 home measurements per day per eye, with an average monitoring period of 8.6 days (standard deviation 1.0). Multiplying those summary figures gives a rough estimate of about 42 readings per eye, but that is a calculation—not the reported total for every participant. () Clinic pressure records included a median of 15.5 visits per eye, spanning nearly five years on average. Office readings came from routine care and could use Goldmann applanation tonometry, a clinic iCare rebound device, or a Tono-Pen. Thus, the clinic data were not all collected with one instrument. () Visual-field progression was estimated from at least three reliable Humphrey visual-field tests using the 24-2 SITA program. Eyes were excluded if there were fewer than three reliable tests or if the first-to-last test interval was less than one year. The average eye had 5.82 visual-field tests (standard deviation 2.82) over a mean follow-up of about 6 years. The mean visual-field mean-deviation slope was −0.49 decibels per year (standard deviation 0.67); the median was −0.18 decibels per year. () The pressure readings themselves The average pressure was similar across home and office measurements: For the full table, please open this article on visualfieldtest.com. The average pressure did not differ significantly across methods (p = 0.62). Other standard summaries did differ across the three measurement contexts. The difference between the pooled home readings and the daily home averages is especially useful to understand: averaging by day compresses extremes. A high or low reading on one day contributes less to the daily-average summary than it does to the all-readings-pooled summary. () The study’s table reports the office standard deviation as 2.91 mmHg with a standard deviation of 2.52; the prose gives 2.62. That small discrepancy does not change the main finding, but it is worth noting when reconstructing the dataset. What PMAT, AIE, and TIE mean The study adapted an idea from continuous glucose monitoring: it asked not only “What is the average?” but also “How often, and by how much, did a reading exceed a chosen limit?” Percentage of measurements above threshold (PMAT): The share of readings above a chosen pressure. If 14 of 100 readings are above the limit, the PMAT is 14%. Average intraocular pressure excess (AIE): How far above the threshold the above-threshold readings were, on average. If readings exceed a 15 mmHg threshold by 1, 2, and 3 mmHg, their average excess is 2 mmHg. Total intraocular pressure excess (TIE): A combined measure of how often and how far readings exceeded the threshold. Repeated or larger exceedances contribute more than rare, small exceedances. The study calculated these measures at 12, 15, 18, and 21 mmHg, and at each patient’s physician-set target. It also calculated home measures in two ways: across the entire monitoring period (“absolute”) and as daily summaries averaged over the monitoring period (“daily”). () Important limitation: PMAT is the percentage of measurements above a threshold, not the percentage of hours or days above it. TIE is not a direct measurement of a continuous “mmHg-hours” pressure dose. Four or five sampled readings in a day cannot reveal exactly how long pressure stayed high between readings—or what happened during sleep. The exact statistical relationships reported A negative coefficient means that a higher pressure metric was associated with a more negative, faster-worsening visual-field slope. It does not mean that raising that metric by one unit causes that amount of damage. Standard pressure measures None of the study’s standard pressure summaries was significantly associated with visual-field slope. The reported coefficients, confidence intervals, and p-values were: For the full table, please open this article on visualfieldtest.com. These are results from the published study’s generalized estimating equation models, which accounted for the fact that some patients contributed both eyes. The models were described as unadjusted association models. () Threshold-based measures The strongest and most consistent signal was for home AIE and TIE at the patient-specific target: For the full table, please open this article on visualfieldtest.com. At fixed thresholds of 12, 15, and 18 mmHg, PMAT, AIE, and TIE were not reported as significantly associated with visual-field progression. AIE at 21 mmHg was also not significant. Office-based versions of the threshold metrics were not significantly associated with progression; office AIE at the individualized target came close but did not meet the conventional significance cutoff (p = 0.053). () The published article’s narrative does not state the exact coefficient and p-value for every nonsignificant threshold-based resul Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/a-360-glaucoma-procedure-beat-simple-needle-goniotomy-at-2-years-how-effective-is-gatt-really Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: A 360° Glaucoma Procedure Beat Simple Needle Goniotomy at 2 Years — How Effective Is GATT Really? Introduction Opening the eye’s natural drainage pathway all the way around sounds as though it should lower pressure more than opening only one small section. A randomized trial published on September 28, 2026 offers a rare direct comparison: gonioscopy-assisted transluminal trabeculotomy, which opens the drainage pathway through 360 degrees, versus a 90-degree procedure using a bent needle. At two years, the full-circle procedure had better average pressure and medication results. But the trial does not prove that treating more degrees alone caused the advantage. The treatments differed in both extent and technique, and the study was small. Its results support gonioscopy-assisted transluminal trabeculotomy as a promising option for selected patients—not as a guarantee of very low pressure or freedom from future treatment. The 2026 randomized trial by Ayub and Costa () What the randomized trial actually studied The trial enrolled 45 eyes from 34 adults at two centers in Brazil. Participants had mild-to-moderate primary open-angle glaucoma, were 40 to 80 years old, had already undergone cataract surgery, and were using no more than three pressure-lowering medicines. Their treated pressure had to be at least 18 millimeters of mercury at two visits. The researchers assigned 23 eyes to gonioscopy-assisted transluminal trabeculotomy (GATT) and 22 to bent ab interno needle goniotomy (BANG). Patients were masked to their procedure, but the surgeons and examiners could identify it. The same experienced surgeon performed all operations. In the full-circle procedure, the surgeon passed a suture around Schlemm’s canal and pulled it through, opening the trabecular meshwork through 360 degrees. The needle procedure removed a strip of tissue over approximately 90 degrees of the nasal angle. So this was not a comparison of the same operation at two different widths: both the instrument and the amount of tissue treated differed. Trial methods and eligibility criteria () Baseline pressure: two different starting points Before surgery, the average pressure while patients were still using their medicines was 19.87 millimeters of mercury in the GATT group and 21.18 in the BANG group. After a medication washout, the averages were much higher and almost identical: 25.43 and 25.55, respectively. The difference between the groups’ treated pressures was not statistically significant, but it matters when interpreting percentage reductions. The average medication burden was also similar: 2.35 medicines in the GATT group and 2.41 in the BANG group. Participants were mostly older adults, with an average age of about 73; the average visual-field loss was mild, and all eyes were pseudophakic, meaning they had an artificial lens after cataract surgery. Baseline data reported for the trial () Two-year results: GATT did better, but the details matter At 24 months, average pressure was 15.41 millimeters of mercury after GATT and 17.79 after BANG. The paper reported reductions from the on-treatment baseline of 22.44% and 16.0%, respectively. Because the GATT group started with a treated average about 1.3 millimeters lower, the difference in the absolute change from those baselines was smaller than the endpoint-pressure gap: approximately 4.46 millimeters of reduction for GATT and 3.39 millimeters for BANG, or roughly 1.1 millimeters more reduction for GATT. The clearest difference was medication use. At two years, the GATT group averaged 0.71 medicines, down from 2.35, while the BANG group averaged 2.26, down from 2.41. That is a reported reduction of 69.78% versus 6.22%. Eleven GATT eyes and two BANG eyes were medication-free. The trial’s “complete success” measure was stricter than simply reaching a particular pressure: an eye needed to be at or below 18 millimeters of mercury, have at least a 20% reduction, and be off medication. “Qualified success” used the same pressure criteria but allowed medication, without increasing the number used at baseline. At 24 months, the paper reported 55.0% complete success after GATT versus 4.5% after BANG. Qualified success was 64.7% versus 13.6% in the article’s results text; its abstract gives 11.4% for BANG. That small inconsistency is worth noting rather than smoothing over. Four GATT eyes reached 12 millimeters of mercury or lower, compared with none after BANG. Four out of 23 randomized GATT eyes is about 17%; four out of 17 GATT eyes completing follow-up is about 24%. Those are simple count-based proportions, not a robust estimate of what an individual patient’s chance would be. The trial’s Kaplan–Meier estimates and its raw eye counts use different methods and denominators. Two-year pressure, medication, target, and success results () Follow-up measurements Patients were scheduled for visits on postoperative days 1, 7, 15, 30, 60, 90, 180, 360, 540, and 720. The journal article’s searchable main text gives exact average pressures at inclusion and at 12 and 24 months. Earlier visit averages were also reported in a conference abstract from the same study. The table below shows those available interim values, with the peer-reviewed journal article’s numbers used for the final 24-month row. The conference report and final paper differ slightly in some late values; the final paper should take precedence. Neither source’s summary gives exact day-15 and day-60 averages. For the full table, please open this article on visualfieldtest.com. Pressure is in millimeters of mercury; figures after ± are standard deviations. The day-1 through day-540 values come from the conference report; final 24-month values come from the journal article. Conference report Final journal article () The pressure rise at day 30 in both groups is a reminder that early postoperative readings can fluctuate. In this trial, medicines were not restarted until day 30; afterwards, treatment was reintroduced under a specified protocol if pressure remained above 18 at consecutive visits. Early and late averages therefore need to be interpreted in light of the medication schedule, not as measurements taken under identical conditions at every visit. Trial follow-up and medication protocol () Loss to follow-up, additional procedures, and safety By 24 months, 19 of 22 BANG eyes and 17 of 23 GATT eyes had completed follow-up. Three BANG eyes left the protocol because they needed additional glaucoma surgery. Six GATT eyes did not complete it: four needed additional surgery, one had a retinal detachment at day 30, and one patient died. Seven eyes had a reoperation: three BANG eyes and four GATT eyes. All three BANG reoperations were bleb needlings; in the GATT group, three were needlings and one was a trabeculectomy. The trial reported no statistically significant difference between groups. Needling is a procedure to revise an existing filtering bleb, so these events should not be read as seven newly created blebs from the angle operations themselves. The study’s failure definition included additional glaucoma surgery. Follow-up and reoperation results () At least one complication was recorded in 12 BANG eyes (54.5%) and 17 GATT eyes (73.9%). Iris damage was the most common complication during surgery, and transient hyphema—blood in the front chamber of the eye—was the most common early postoperative problem. One GATT eye had a total hyphema on day one; it cleared within a week without intervention. The retinal detachment occurred 30 days after GATT, but one event in a small study cannot establish that the operation caused it. The article also reported a BANG eye with persistent corneal edema and cystoid macular edema associated with vitreous prolapse and a poorly positioned artificial lens. Some eyes in both groups showed notable reductions in corneal endothelial-cell counts. At two years, average counts were 1,561.88 cells per square millimeter after GATT and 1,477.56 after BANG; the difference between groups was not statistically significant. At least a 20% reduction occurred in 30.4% of GATT eyes and 22.7% of BANG eyes. These small-sample findings warrant follow-up; “no significant difference” does not establish that either procedure has no effect on the cornea. Complications and endothelial-cell results () Does opening more degrees produce more pressure reduction? Why a 360-degree opening might help The trabecular meshwork is part of the eye’s main fluid-drainage route. In open-angle glaucoma, resistance in this pathway is often too high. GATT opens the meshwork around the full circumference of Schlemm’s canal, whereas the trial’s BANG procedure treated about 90 degrees. A wider opening could help by reducing resistance over a larger area, reaching more of the eye’s drainage channels, and providing alternative routes if some regions drain poorly. Outflow is uneven around the eye, so a small opening may happen to reach a less useful region—or it may reach a particularly effective one. Healing and scarring could also affect how long any opening stays useful. These are plausible explanations, not mechanisms proven by this trial. Trial discussion of treatment extent and regional drainage () The broade Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/the-largest-glaucoma-genome-study-yet-found-29-new-genetic-clues-could-existing-drugs-target-some-of-them Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: The Largest Glaucoma Genome Study Yet Found 29 New Genetic Clues — Could Existing Drugs Target Some of Them? The short answer is possibly—but the study did not identify a ready-made glaucoma drug. It found genetic associations that point toward several plausible disease mechanisms, including extracellular-matrix remodeling, aqueous-fluid outflow, cellular stress responses and retinal ganglion-cell survival. Among the four highlighted drug targets, the mammalian target of rapamycin pathway has the strongest combination of genetic, experimental and drug-delivery evidence. Even there, the right direction and amount of treatment remain uncertain. A critical distinction: a gene associated with glaucoma is not automatically a treatment target. The genetic finding may not reveal what the variant does, which eye cell it affects, or whether a drug should increase or decrease the gene’s activity. The paper itself cautions that, for most of these associations, pharmacological direction cannot yet be predicted. () This article distinguishes established evidence—what the studies directly report—from strong inference and informed speculation about possible treatments. What the study actually found The Communications Biology paper was published online on September 23, 2026. Its early-access version is peer reviewed but still described by the publisher as an article in press that may receive further edits. It is a genetic-association study, not a clinical trial. () Cohorts and ancestry For the full table, please open this article on visualfieldtest.com. The discovery and replication sequencing analyses were restricted to participants of European ancestry. The paper says 464,778 European-ancestry participants made up about 95% of its UK Biobank whole-genome-sequencing resource. The All of Us replication sample was also European ancestry. FinnGen represents a Finnish population, while the Million Veteran Program is ancestrally diverse overall, but the study’s cited open-angle-glaucoma analysis used its European-ancestry results. Thus, the large headline sample does not mean that the principal discovery and replication findings were tested across equally large, diverse ancestry groups. () The authors also report a preliminary UK Biobank pan-ancestry analysis that found 15 additional significant variants—11 rare and four common. They had external replication evidence for only one of those, a common variant near ADGRB2. The authors note that many signals were not present or testable in current external datasets. () Important caveat: the replication phenotype was broader than the discovery phenotype In UK Biobank, cases were identified from self-reported glaucoma and medical-record codes, with secondary forms excluded. In All of Us, the researchers used medical-record codes for glaucoma because that definition had more cases and greater statistical power than the smaller primary open-angle glaucoma-specific definition. This means the replication check was not a perfect match to the primary open-angle glaucoma discovery phenotype. FinnGen used a primary open-angle glaucoma endpoint; the Million Veteran Program used an open-angle-glaucoma phenotype. () That does not invalidate the replication evidence, but it makes the word “replication” less straightforward than it may sound. A signal that appears in a broader glaucoma group is supportive; it is not the same as reproducing the exact association in an independently diagnosed primary open-angle glaucoma cohort. Sequencing, variant thresholds and statistical significance The UK Biobank genomes were sequenced on an Illumina NovaSeq 6000 platform at an average depth of about 32.5-fold. The researchers used GraphTyper-called single-nucleotide variants and insertions or deletions, applied quality filters, and used REGENIE, a method designed to account for population structure and relatedness. Single-variant analyses included variants with a minor allele count of at least five and tested variants within genes, including a one-kilobase margin; intergenic variants were excluded. () The paper categorizes variants with an effect-allele frequency below 1% as rare. For single-variant tests, genome-wide significance was P 5 × 10⁻⁸. For gene-based rare-variant tests, the threshold was P 2.5 × 10⁻⁶, based on correction for roughly 20,000 genes. The gene-based analysis used loss-of-function variants and, in another test, combined loss-of-function, missense and nearby regulatory variants. () For external checks, the authors looked up significant variants and genes in All of Us, FinnGen and the Million Veteran Program. If an exact rare variant was not available, they sometimes counted a significant variant elsewhere in the same gene region as support. The methods do not describe one uniform, strict replication threshold applied to every variant and gene. The paper’s “replicated or supported” label therefore covers different kinds and strengths of evidence. () The “29 new clues” were not 29 new genes The study reports 29 novel genome-wide significant rare-variant associations. That is not the same as finding 29 new glaucoma genes. The complete table contains 36 genome-wide significant rare variants, including established variants in MYOC and OPTN. A gene may contain a rare association without the study proving that the gene itself is the causal effector. () Among the highlighted novel rare variants were: For the full table, please open this article on visualfieldtest.com. The paper also confirmed known rare-variant associations in MYOC and OPTN. These confirmations help show that the analysis can recover established biology; they are not new treatment findings. () Gene-based testing identified six significant genes: DDR2, MYOC, LTBP2, MTOR, ANGPTL7 and FKBP9. The paper described new gene-based associations for DDR2, LTBP2, MTOR, ANGPTL7 and FKBP9, while MYOC is already an established glaucoma gene. The gene-based associations for DDR2 and LTBP2 came from loss-of-function variants; MTOR, ANGPTL7 and FKBP9 were identified using broader variant sets. () The paper also reported common-variant associations in 22 genes not previously reported as gene-level primary open-angle glaucoma associations. MAPT appears in a common-variant signal near the KANSL1/MAPT region. LYN, by contrast, is highlighted in connection with a rare single-variant association. These are different kinds of evidence and should not be treated as equally precise gene identifications. () What biology do the new signals point toward? The researchers examined gene-expression datasets from ocular tissues and cell types. They found evidence that many associated genes are expressed in trabecular-meshwork cells, Schlemm’s canal, retinal ganglion cells, retinal support cells, or optic-nerve and posterior-eye tissues. That supports biological plausibility, but expression does not prove that a gene causes glaucoma. The expression analyses were based on existing datasets, not new experiments in diseased human eyes. () The most plausible biological interpretations Aqueous outflow and intraocular pressure: LTBP2, ANGPTL7, DDR2, PRRX1 and TNS3 are plausible candidates for effects on connective tissue, cell attachment, extracellular matrix or outflow-pathway remodeling. The trabecular meshwork is a major site of resistance to aqueous-fluid drainage, and Schlemm’s canal helps carry that fluid out of the eye. () Retinal ganglion-cell resilience and axon health: MTOR, PRRC2C, METTL13/EEF1AKNMT and some of the other associated genes are plausible participants in cellular stress responses, protein production, or the survival of retinal neurons and their axons. Several associated genes were detectable in retinal ganglion cells or retinal support cells. () Metabolism and vascular biology: FMO3 is primarily a liver enzyme involved in metabolism of trimethylamine. The paper proposes a possible systemic route involving trimethylamine N-oxide and vascular function, but this is not evidence that the glaucoma-associated variant acts in the eye. () Glial and inflammatory biology: The paper found expression of genes including LYN, MTOR and PRRC2C in retinal Müller glia or astrocytes. These cells support retinal neurons and participate in stress responses. Expression alone cannot show whether their activity is protective or harmful in glaucoma. () Functional predictions are leads, not measurements The authors used AlphaGenome, a computational model that predicts effects on features such as gene regulation, chromatin accessibility and splicing. Among 29 novel rare variants analyzed, 12 had at least one predicted effect above the paper’s threshold in an eye-related tissue or cell type. Predictions for METTL13 and DNM3 included trabecular-meshwork effects; the FMO3 variant had a predicted splice-related effect. The authors state that they did not experimentally validate these predictions. A model-predicted increase or decrease in an assay track also does not, by itself, establish that the gene’s activity increased or decreased in the relevant living eye cell. () Four drug-highlighted genes: what might—and might not—be actionable? The paper used the Open Targets platform to identify genes with e Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/can-air-pollution-damage-the-optic-nerve-a-large-review-links-pm2-5-to-higher-glaucoma-risk Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Can Air Pollution Damage the Optic Nerve? A Large Review Links PM2.5 to Higher Glaucoma Risk The short answer: Long-term exposure to fine particulate matter, or PM2.5, is associated with glaucoma in several populations, and there are plausible ways pollution could affect the eye’s blood supply and nerve cells. But the new European Society of Cataract and Refractive Surgeons analysis is available publicly mainly as a conference announcement—not a full methods paper. Its headline figures cannot yet be checked or translated reliably into a specific change in air pollution concentration. The evidence makes PM2.5 a credible candidate modifiable risk factor, not an established cause of glaucoma. It is reasonable to reduce avoidable exposure when doing so is practical, especially for general health. There is no evidence that an air purifier prevents glaucoma or slows vision loss. What the ESCRS 2026 analysis actually reported The study, presented on September 14, 2026, was titled “Smog and sight: epidemiological evidence on the link between air pollution and ocular aging: a comprehensive systematic review and meta-analysis.” The European Society of Cataract and Refractive Surgeons reported that it included 41 observational studies and data from millions of people, described as coming mainly from East Asia and the United Kingdom. The review considered glaucoma, cataract, and age-related macular degeneration, and examined fine and larger particulate matter, nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide. () The 41 studies were not reported as 41 glaucoma studies. They were the total for the review’s eye-disease outcomes. The public announcement does not give the number of glaucoma studies, the exact participant count, the search dates, study-selection rules, pooled model details, pollutant-specific concentration ranges, confidence intervals, or study-quality ratings. The cited conference abstract is identified by number, but I could not verify those details in a full accessible report. The headline findings therefore warrant interest, but they cannot yet be audited in the same way as a full journal article. () The ESCRS announcement says that people in the most polluted areas had up to 70% higher odds of glaucoma than those in the least polluted areas. It also reports that glaucoma risk rose by about 8% for each “meaningful step” up in pollution exposure. The announcement does not define that step as an interquartile-range increase, provide a common PM2.5 increment in micrograms per cubic meter, or give a confidence interval for the 8% figure. So the claim that the ESCRS analysis found a pooled odds ratio of 1.08 per interquartile-range increase is not verifiable from its public summary. () A separate 2026 glaucoma-specific review provides useful context, but it is not the ESCRS review. Its abstract reports 18 observational studies, with eight contributing to a PM2.5 meta-analysis. The pooled relative-risk estimate was 1.12, with substantial between-study variation (I² = 78.7%). That result supports an association, but the abstract does not provide a single shared concentration increment that would let readers convert the estimate into one universal number of micrograms per cubic meter. () What does “per interquartile-range increase” mean? The interquartile range is the difference between the 75th-percentile and 25th-percentile exposure levels within a study. An estimate “per interquartile-range increase” means comparing an exposure one study-specific interquartile range higher with the exposure before that increase. That is useful for analyzing each study, but it does not create a common dose across studies. An interquartile range of about 1 microgram per cubic meter is very different from one of 2.9 micrograms per cubic meter. A percentage increase “per interquartile range” therefore cannot be translated into a fixed PM2.5 concentration unless the study’s own interquartile range is known. Examples from published research illustrate the problem: A United Kingdom Biobank analysis reported an odds ratio of 1.06 per interquartile-range increase in PM2.5; the increment was about 1.1 micrograms per cubic meter in that analysis. A related analysis found higher odds of self-reported glaucoma and differences in retinal structure. () A Canadian Longitudinal Study on Aging analysis reported an odds ratio of 1.14 per interquartile-range increase, with the increment reported as about 2.9 micrograms per cubic meter in a systematic review of the study. () A large rural Chinese study reported an odds ratio of 1.07 per 10 micrograms per cubic meter—a fixed increment, not an interquartile range. () A Taiwanese study used yet another measure: cumulative exposure categories based on PM2.5 levels multiplied by months of exposure. Its highest category had an odds ratio of 1.67 compared with its reference category. Those categories are not equivalent to a person breathing an annual average that is a fixed number of micrograms per cubic meter higher. () Bottom line: An interquartile-range result is meaningful only alongside the underlying exposure range. The ESCRS summary does not report enough information to translate its 8% figure into a dependable concentration change. Odds, relative risk, and absolute risk are different The ESCRS summary’s “70% higher odds” is a relative comparison between exposure groups, not a 70-percentage-point increase in the chance that any one person will get glaucoma. An odds ratio compares the odds of an outcome in one group with the odds in another. A relative risk compares their probabilities. For uncommon outcomes, odds ratios and relative risks can be numerically close, but they are not identical. An individual’s absolute risk also depends on their starting risk, which is affected by factors such as age, family history, and other health characteristics. For illustration only: if a group’s starting risk were 2%, an odds ratio of 1.67 would correspond to a risk of about 3.3%, not 72%. This calculation is not an estimate of the risk in the Taiwanese study or in a particular patient; it simply shows why “70% higher odds” does not mean “70% chance of glaucoma.” In the United Kingdom prospective cohort discussed below, roughly 2% of participants developed glaucoma over a median 12.8 years, but that rate should not be applied to every population. () The “up to 70%” figure should therefore be read as a highest-versus-lowest exposure comparison reported in the conference summary, not as a typical effect for every rise in pollution. A specific underlying Taiwanese study found an odds ratio of 1.67 for its highest cumulative exposure category versus its reference category; the available ESCRS summary does not establish that this was the source of its 70% figure or give enough detail to equate the comparisons. () What do the underlying studies show? The evidence is not limited to the conference announcement. Several earlier studies reported positive associations, although they differ in how they measured pollution and glaucoma. Studies with stronger or more objective designs The most useful epidemiological support comes from studies that follow people over time or use clinical examinations rather than relying only on self-report: United Kingdom Biobank, 12-year follow-up: Among 448,253 participants in the particulate-matter analysis, 8,999 incident glaucoma cases were identified over a median 12.8 years. After the study’s broadest adjustment, each study-specific interquartile-range increase in PM2.5 was associated with a 3% higher hazard of glaucoma (hazard ratio 1.03, 95% confidence interval 1.00–1.06). People in the highest exposure quartile—10.57 to 21.31 micrograms per cubic meter—had a 10% higher hazard than those in the lowest quartile—8.17 to 9.29 micrograms per cubic meter. The continuous estimate was small and just met the conventional threshold for statistical significance; the quartile comparison was also modest. () Rural China: In a cross-sectional study of 33,701 adults, each 10-microgram-per-cubic-meter higher PM2.5 level was associated with an odds ratio of 1.07 for glaucoma, with a confidence interval reaching 1.00. The same study reported a larger estimate for primary angle-closure glaucoma, illustrating that subtype findings may differ. () Canada: In the Canadian Longitudinal Study on Aging, higher PM2.5 was associated with glaucoma after adjustment for sociodemographic and health factors. A positive association was also reported in a model that included multiple pollutants, although the study was cross-sectional and its outcomes included self-reported diagnoses. () United Kingdom Biobank, earlier analyses: An earlier analysis found higher odds of self-reported glaucoma with greater PM2.5 exposure. Because exposure and glaucoma status were assessed in a population-based cohort rather than through long-term follow-up of new diagnoses, it cannot establish which came first. () These findings are directionally consistent: several studies found more glaucoma diagnoses or glaucoma-related structural changes at higher PM2.5 exposure. But studies differ in design and outcome, and the 2026 glaucoma-specific review reported high heterogeneity. The po Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/ai-found-21-new-genetic-clues-to-glaucoma-could-some-become-future-drug-targets Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: AI Found 21 New Genetic Clues to Glaucoma — Could Some Become Future Drug Targets? A study published in npj Genomic Medicine on September 19, 2026 used artificial intelligence to look for glaucoma-related patterns in optical coherence tomography scans, then tested those patterns against genetic data. The researchers reported 21 genetic loci not previously linked to glaucoma, and prioritized 11 genes that might help explain why glaucoma damages the eye. Five of those genes had not previously been reported in glaucoma research. () The work’s main advance is not that artificial intelligence diagnosed glaucoma better. It is that the researchers used measurable patterns of retinal damage—rather than a simple “glaucoma” or “no glaucoma” label—to search for genetic clues. That approach produced a richer biological picture, including a particularly promising signal involving RSPO2 and Wnt signaling in cells that help drain fluid from the eye. But these are genetic leads, not tested glaucoma treatments. The study did not show that changing any of the 11 genes prevents vision loss. The most exciting possibilities still require experiments to establish which genes are truly involved, whether changing them would help or harm, and whether a treatment can reach the right cells safely. What the study found—and what it did not The peer-reviewed article is “Deep-learning-derived glaucoma-related endophenotypes enable novel genome-wide genetic and functional discovery”. It reports 36 genome-wide significant loci in the European-ancestry analysis and 43 in a cross-ancestry analysis. The authors identified 21 loci as previously unreported in glaucoma and used additional analyses to prioritize 11 genes, five of them novel to glaucoma. () A locus is a region of the genome associated with a trait; it may contain several genes. A gene prioritized at a locus is a candidate for explaining the association, not necessarily the gene that causes it. The study therefore offers a set of hypotheses about glaucoma biology. It does not establish that the 21 loci—or any of the 11 genes—cause glaucoma, nor that a drug aimed at them would work. The methodological innovation, in patient-friendly language From a yes-or-no label to a detailed retinal “fingerprint” Many genetic studies classify each participant as having glaucoma or not having glaucoma. That can be a noisy comparison: some people may have undiagnosed disease, and people with glaucoma can have very different patterns and amounts of retinal damage. Instead, these researchers trained machine-learning models on eye scans from people with glaucoma. The models learned patterns in the ganglion cell complex and retinal nerve fiber layer—retinal structures that are affected as glaucoma damages the optic nerve. They then represented those patterns as quantitative traits, or measurable features of the scans. A useful analogy is the difference between asking whether a house is “damaged” and measuring exactly where its walls are cracked, how deep the cracks are, and how much the structure has shifted. The detailed measurements can reveal more about the process behind the damage. These scan-derived traits, which the researchers call endophenotypes, were then linked to genetic differences. They are glaucoma-informed measurements, not a replacement diagnosis or a measure of future vision loss. The study’s full-text manuscript describes two machine-learning model families, labelled AUTO and MOCO, used to produce traits from macular scans. () Reconstructing the research pipeline Train on glaucoma scans: The models were developed using 18,985 clinical optical coherence tomography scans from 8,323 glaucoma patients at Mass Eye and Ear. The earlier manuscript says most had open-angle glaucoma codes, though the training group was not restricted to chart-confirmed primary open-angle glaucoma cases. () Apply the models to UK Biobank: The final peer-reviewed publication reports 39,146 UK Biobank participants with usable genetic and scan-derived data. The ancestry groups were 35,739 European, 1,730 African, and 1,677 Asian participants. The large difference in group sizes means the European results had much greater statistical power. () Run genome-wide association studies: The researchers tested genetic variants against 21 scan-derived traits, separately by ancestry. A genome-wide association study looks across the genome for variants statistically associated with a measured trait. Split samples for discovery and replication: The manuscript describes a 75% discovery / 25% replication split within UK Biobank, followed by meta-analysis. This is useful internal checking, but it is not the same as replication in a fully independent cohort. () Combine results across ancestry groups: They conducted ancestry-specific analyses and then a cross-ancestry meta-analysis, finding 36 significant loci in the European analysis and 43 in the cross-ancestry analysis. Smaller African and Asian sample sizes limit how confidently those group-specific effects can be estimated. Prioritize possible genes and mechanisms: Follow-up analyses included gene-based testing, expression and splicing quantitative trait loci (eQTLs and sQTLs), Bayesian colocalization, Mendelian randomization, and single-cell expression enrichment in eye tissues. These analyses help narrow a locus to possible genes and cell types, but each has its own assumptions and limitations. () Which UK Biobank number should be used? The peer-reviewed publication’s figure is 39,146 participants. An earlier medRxiv abstract reported 47,908, but the manuscript’s detailed ancestry counts—35,739 + 1,730 + 1,677—sum to 39,146. The final publication’s participant number should be used for the peer-reviewed study. The public versions do not clearly explain the origin of the earlier headline figure, so it is safest to treat it as an earlier or inconsistent version figure rather than assume it represents the final analysis. () What “21 new genetic clues” means The authors call 21 loci novel to glaucoma because they had not previously been reported as associated with glaucoma or established glaucoma-related traits. “Novel” here does not mean the genes were newly discovered, that the DNA changes are unique to glaucoma, or that the genes’ roles in the body are now understood. The 11 prioritized genes were: EIF3E, LIN52, NPLOC4, PBLD, RSPO2, SLC25A16, TSPAN10, DYNC1I2, SLC25A12, ATOH7, and C14orf39. The paper identifies RSPO2, EIF3E, LIN52, DYNC1I2, and SLC25A12 as the five genes not previously reported in glaucoma. It also notes prior glaucoma-related or eye-trait evidence for some of the other genes, including ATOH7, C14orf39, NPLOC4, TSPAN10, PBLD, and SLC25A16. () The 11 prioritized genes: biology, eye-cell evidence, and drug prospects The cell evidence below refers to the study’s expression and enrichment analyses—not proof that a gene causes disease in that cell. The single-cell reference data came from non-diseased human eye tissues, and for several genes the article does not identify a particular eye-cell type as the key location. () For the full table, please open this article on visualfieldtest.com. Two shared regions make some gene assignments especially uncertain Several prioritized genes sit in the same genetic region. For example, DYNC1I2 and SLC25A12 share a locus in the study’s prioritization table; both may be plausible candidates, but the association does not establish which gene—or whether both—accounts for the signal. A similar caution applies to the chromosome 10 region involving ATOH7, PBLD, and nearby genes. These are reasons for follow-up experiments, not reasons to discard the findings. () The main biological themes Wnt signaling and aqueous outflow: the clearest treatment-oriented lead Aqueous humor is the clear fluid inside the eye. It normally drains through the trabecular meshwork. If drainage meets too much resistance, eye pressure can rise. Lowering pressure is an established way to slow glaucoma damage. RSPO2 is notable because it can strengthen Wnt signaling and the study found it in trabecular-meshwork and other anterior-segment fibroblasts, as well as optic-nerve-head fibroblasts. That puts a biologically plausible candidate in cells involved in tissue structure and outflow. Importantly, earlier laboratory work supports a role for canonical Wnt signaling in the trabecular meshwork and pressure regulation. In experimental models, blocking Wnt signaling raised pressure, and another study found that Wnt activation could reverse some abnormal features of trabecular-meshwork cells. Those results strengthen the general Wnt–outflow hypothesis—but they do not prove RSPO2 causes glaucoma or establish whether RSPO2 itself should be increased or decreased. () That direction matters. RSPO2 boosts Wnt signaling, and the prior eye studies suggest that too little canonical Wnt activity may be harmful in the trabecular meshwork. A simple plan to block RSPO2 could therefore be wrong. The best therapeutic idea, if the genetics is confirmed, may be to restore or tune local Wnt signaling, rather than turn it off across the body. Retinal ganglion-cell vulnerability, axonal transport, and mitochondria The study’s cross-ancestry gene-expression enrich Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/preserflo-vs-trabeculectomy-a-new-randomized-trial-tests-which-glaucoma-surgery-really-lowers-pressure-better Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: PRESERFLO vs Trabeculectomy: A New Randomized Trial Tests Which Glaucoma Surgery Really Lowers Pressure Better The new trial reports an important change over time: PRESERFLO had lower pressure early after surgery, while trabeculectomy achieved lower pressure at 3 and 12 months. But the published abstract does not provide the exact pressure values or confidence intervals needed to calculate the size of that difference. Here is what the study does—and does not—establish. The short answer The new trial supports trabeculectomy as the stronger pressure-lowering choice when the main goal is a very low pressure. It does not show how many millimeters of mercury a patient gives up by choosing PRESERFLO, because its abstract does not provide the arm-by-arm pressure readings needed to calculate that difference. Across earlier comparative evidence, the average long-term pressure advantage for trabeculectomy has generally been about 1 to 3 mmHg. That difference may matter more when glaucoma is advanced and the target is in the low teens—or lower. PRESERFLO remains a reasonable option for some people whose target is less stringent and who value its design and potential reduction in certain postoperative risks. But it is still bleb-forming filtration surgery: it is not free of scarring, needling, follow-up, or late infection risk. The new trial was published on September 19, 2026, just five days before this article’s date, September 24, 2026. It is an accepted, early online article that may receive final editorial changes. It randomized 99 people: 51 to PRESERFLO MicroShunt with mitomycin C and 48 to trabeculectomy with mitomycin C. The abstract reports lower early pressure with PRESERFLO and lower pressure with trabeculectomy at 3 and 12 months. () What the new randomized trial did Who was studied—and what we can verify The study included adults with primary open-angle glaucoma (POAG) or pseudoexfoliation glaucoma (PEXG) whose disease was progressing despite maximum tolerated treatment. Eligibility required worsening visual-field results and pressure remaining above the patient’s target despite topical and oral medicines. The study was conducted at one center in Poland, with recruitment from April 2023 to October 2024 and 12 months of follow-up. () Some details requested by patients—including the exact numbers of POAG versus PEXG participants, the distribution of glaucoma severity, mean baseline pressure, average number of baseline medications, and the numerical target pressure—are not included in the searchable abstract and methods text available for this review. The full paper may contain additional figures or tables, but those values are not reproduced here rather than guessed. The study says that disease progression was assessed with visual fields, but that alone does not establish how many participants had mild, moderate, or advanced damage. () How surgery and randomization were handled The researchers used folded allocation slips to assign patients in a 1:1 ratio immediately before surgery. The slips were prepared by an investigator who did not enroll participants. There was no blocking or stratification, and neither surgeons nor participants could be blinded; outcome assessors were not formally blinded either. The study was registered after recruitment had begun: the paper says registration occurred on March 16, 2026, after enrollment ended in October 2024. The authors say the protocol and analysis plan had been set before recruitment. Retrospective registration and unblinded assessment do not invalidate the findings, but they are reasons to interpret a small, single-center trial cautiously. () A single experienced surgeon performed the procedures. Mitomycin C (MMC) was applied with sponges for two minutes at either 0.2 mg/mL or 0.4 mg/mL, with the concentration chosen by the surgeon based on anticipated scarring risk. In the trabeculectomy group, the surgeon created a scleral flap, used a Kelly punch, and secured the flap with four nylon sutures. In the PRESERFLO group, no intraluminal stent or ripcord was used. Cataract surgery was combined with filtration surgery in 37 of 51 PRESERFLO cases and 33 of 48 trabeculectomy cases. () Patients continued their glaucoma medicines through the day of surgery; there was no medication washout. The study used antibiotic and steroid treatment after surgery. Both procedures still require postoperative assessment of pressure and the filtering bleb; the exact medication-adjustment and visit schedule is not available in the abstracted text. () Pressure results: what is known and what is not The published abstract reports the direction of the result, but not the exact mean pressures, standard deviations, confidence intervals, or between-group effect sizes for each visit. The table below separates what the abstract says from numbers that cannot be verified from it. For the full table, please open this article on visualfieldtest.com. These are reporting limits of the abstracted information, not evidence that the full paper contains no numerical table. Without arm-specific baseline and follow-up means—and their variability—it is not possible to calculate reliable absolute reductions, percentage reductions, confidence intervals, or a standardized effect size for this 99-person trial. Nor is it possible to infer how many individuals crossed a particular pressure threshold from a group average. () How large is the pressure difference in the broader evidence? The new study fits a pattern already seen in comparative research. A 2025 meta-analysis of 10 comparative studies found that trabeculectomy achieved a mean pressure about 1.59 mmHg lower than PRESERFLO and a larger pressure reduction from baseline. A later meta-analysis covering 14 studies and 2,229 patients estimated that pressure after PRESERFLO was 1.44 mmHg higher than after trabeculectomy (95% confidence interval, 0.64 to 2.24 mmHg); pressure reduction was 2.73 mmHg smaller with PRESERFLO (95% confidence interval, 1.61 to 3.84 mmHg smaller). These pooled results had moderate-to-high variation between studies and largely reflect follow-up of up to two years—not a guaranteed difference for an individual patient. () The largest earlier randomized comparison enrolled 527 people with POAG: 395 received PRESERFLO and 132 trabeculectomy. At one year, reported mean pressure reductions were 29.1% with PRESERFLO and 45.4% with trabeculectomy. Surgical success—defined in that trial as at least a 20% reduction from baseline without increasing medicines—was also lower in the PRESERFLO group at one year. This was a different trial, with different participants and methods, so its figures should not be substituted for the new trial’s missing values. () Bottom line on pressure: The comparative evidence generally favors trabeculectomy for achieving the lowest pressure. The best pooled estimate is a difference of roughly 1 to 2 mmHg in postoperative pressure, with some studies showing a larger gap. The new randomized trial adds support to that direction, but the abstract alone does not tell us the trial’s exact difference. Why the early result could reverse Mechanistic explanation—inference, not a finding proven by the trial: PRESERFLO is an 8.5-millimeter tube with a 70-micrometer lumen. That lumen creates resistance to fluid flow and is intended to reduce excessive early drainage. Trabeculectomy instead makes an opening beneath a surgically fashioned scleral flap, which the surgeon can adjust using sutures; those sutures can sometimes be loosened or cut with laser after surgery. The two operations therefore manage early flow differently. () A lower pressure immediately after PRESERFLO surgery does not necessarily mean it will maintain a lower pressure later. As healing proceeds, scarring around the tube outlet or within the bleb can restrict drainage. A trabeculectomy may, by contrast, be adjusted after surgery to improve filtration. The main trial’s findings are consistent with these possible explanations, but they do not prove that the tube’s fixed lumen or bleb scarring caused the reversal. Differences in postoperative adjustment, steroid treatment, healing, or the cataract operations performed alongside filtration surgery could also contribute. The trial did not use a PRESERFLO intraluminal stent, and it used MMC at the surgeon’s choice of two concentrations. Because the dose varied, any claim that the results demonstrate a single optimal MMC exposure—or that MMC explains the reversal—would go beyond the reported evidence. () Complete and qualified success: useful, but not enough on its own Complete success usually means reaching a specified pressure target without glaucoma medicines. Qualified success means reaching the target with medicines permitted. These labels are only meaningful when the pressure cutoff, required percentage reduction, and rules for further surgery are clear. For the new trial, the abstract says complete success at six months was significantly higher after trabeculectomy and that qualified success was comparable between groups over follow-up. It does not give the exact percentages or the pressure thresholds behind those results. So it can Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/can-an-implant-free-laser-procedure-free-glaucoma-patients-from-eye-drops-new-2-year-elios-results Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Can an Implant-Free Laser Procedure Free Glaucoma Patients From Eye Drops? New 2-Year ELIOS Results Bottom line The new 24-month ELIOS excimer laser trabeculostomy results are encouraging—but they answer a narrower question than many headlines suggest. The study shows that cataract surgery combined with ELIOS can produce a sustained reduction in unmedicated eye pressure and allow many patients to stop glaucoma drops for at least two years. In the pivotal study, mean unmedicated diurnal eye pressure fell from approximately 24.5 millimeters of mercury at baseline to 16.8 millimeters of mercury at 24 months, and 82.0% of patients were medication-free around month 23. Gallardo et al., 24-month pivotal study () However, the central limitation is important: there was no concurrent cataract-surgery-only control group. The trial was a prospective, single-arm study that compared its results with historical performance goals derived from earlier minimally invasive glaucoma surgery trials. My interpretation is: ELIOS plus cataract surgery works as a combined treatment. It probably provides additional pressure lowering beyond cataract surgery alone. The most reasonable estimate of the additional ELIOS effect at 24 months is approximately 1.5 to 2.5 millimeters of mercury, with a plausible range of roughly 1 to 3 millimeters of mercury. The medication-free benefit may be real and clinically valuable, but the exact size of that benefit is less certain without a randomized control arm. ELIOS appears best suited to patients with mild-to-moderate primary open-angle glaucoma who already need cataract surgery. It should not be viewed as a replacement for trabeculectomy or tube surgery in patients needing an eye pressure below 12 millimeters of mercury, or in many patients with advanced glaucoma. The original paper was published online on September 8, 2026, and the two-year results were presented at the European Society of Cataract and Refractive Surgeons Congress in London from September 10 through September 14, 2026. () What is ELIOS? ELIOS is an implant-free form of excimer laser trabeculostomy. Instead of leaving a stent inside the eye, the procedure uses a 308-nanometer xenon chloride excimer laser to create small openings through the trabecular meshwork, the eye’s main drainage tissue. These openings are intended to provide a more direct route for fluid to enter Schlemm’s canal and then reach the eye’s natural collector channels. The current ELIOS treatment creates: 10 microchannels Each approximately 210 micrometers in diameter Across approximately 90 to 110 degrees of the nasal trabecular meshwork After cataract removal and placement of an intraocular lens The procedure is performed through a small corneal incision under gonioscopic visualization. It is described as nonthermal photoablation, meaning that tissue is removed by breaking molecular bonds rather than by burning or coagulating tissue. () The 2026 pivotal study: exact design Study design The pivotal trial was: Prospective Multicenter Nonrandomized Single-arm Conducted under a United States investigational device exemption Registered as NCT04899063 Conducted at 20 United States sites Treatment period: approximately June 2021 through July 2023 Published as a 24-month report in Ophthalmology Glaucoma The study included 318 patients who underwent cataract surgery followed by ELIOS. ClinicalTrials.gov study record () How many patients completed 24 months? This point requires careful wording. The original paper’s abstract reports 318 treated patients and presents the 24-month efficacy percentages using figures that correspond closely to a 318-patient denominator: 84.2% at 12 months corresponds to approximately 268 of 318 76.1% at 24 months corresponds to approximately 242 of 318 82.0% medication-free around month 23 corresponds to approximately 261 of 318 A conference report described the study as involving 318 patients who completed the two-year cohort, but the PubMed abstract does not provide a separate conventional patient-flow table showing enrollment, losses to follow-up, exclusions, and the exact number available at every visit. Therefore, the most defensible statement is: > 318 patients underwent the combined procedure, and the published endpoint percentages appear to use the 318-patient analysis population; the publicly visible abstract does not separately document a detailed 24-month completer denominator. That distinction matters because a study can report an analysis percentage based on available or imputed data without every patient completing every examination. () Who was included? The study enrolled adults who had: Age of at least 45 years Mild-to-moderate primary open-angle glaucoma An operable age-related cataract Best-corrected visual acuity of approximately 20/40 or worse, according to the trial eligibility description Medicated eye pressure of 24 millimeters of mercury or less Treatment with one to three glaucoma medications Unmedicated mean diurnal eye pressure between 22 and 34 millimeters of mercury after medication washout The study therefore did not primarily test ELIOS in patients with advanced disease, very low target pressures, or highly medication-resistant glaucoma. () Baseline medication use The mean baseline medication burden reported in the 12-month conference abstract was approximately: 1.5 medications Standard deviation approximately 0.7 medications This is important. The study population was not made up mainly of patients taking four or five medications. It was largely a mild-to-moderate glaucoma population with a modest medication burden. () Baseline eye pressure The study reported: Mean medicated eye pressure at screening: 17.05 ± 3.01 millimeters of mercury Mean unmedicated diurnal eye pressure at baseline: 24.53 ± 2.51 millimeters of mercury The unmedicated diurnal measurement was taken after glaucoma medications had been stopped according to the study protocol. () Washout protocol The public abstract confirms that patients had to reach the required unmedicated diurnal eye pressure range after washout. However, the abstract does not list the exact medication-specific washout durations—for example, the number of days required for prostaglandin analogues, beta blockers, or carbonic anhydrase inhibitors. That information should not be inferred from another trial. Hydrus and iStent pivotal trials also used medication washouts, but their exact schedules and visit procedures were not necessarily identical to those used in ELIOS. The ELIOS publication therefore supports the statement that the baseline pressure was measured after medication washout, but the publicly available abstract does not allow a complete reconstruction of the washout timetable. () Cataract-surgery procedure Patients underwent: Standard phacoemulsification cataract extraction Placement of an intraocular lens ELIOS excimer laser trabeculostomy after the cataract portion was completed The trial therefore studied a combined operation, not ELIOS in isolation. () The prespecified primary endpoints The study had two co-primary efficacy endpoints at both 12 and 24 months. Endpoint 1: percentage achieving at least a 20% pressure reduction The percentage of patients had to achieve at least a 20% reduction in unmedicated mean diurnal eye pressure from baseline. The prespecified performance goals were: 12 months: greater than 79% 24 months: greater than 68.5% Endpoint 2: mean change in unmedicated diurnal eye pressure The mean reduction in unmedicated diurnal eye pressure had to meet: 12 months: at least 7.2 millimeters of mercury 24 months: at least 6.15 millimeters of mercury These were not comparisons against a contemporaneous cataract-only group. They were comparisons against historical performance goals derived from cataract-only arms in prior minimally invasive glaucoma surgery trials. () Exact 24-month results The results reported in the original paper were: For the full table, please open this article on visualfieldtest.com. The 12-month result represented approximately a 34.5% reduction, while the 24-month change represented approximately a 30% reduction from the washed-out baseline pressure, depending on whether one uses the reported group means or the paired endpoint estimates. A small arithmetic issue is worth noting: the reported mean pressure at each visit does not subtract exactly from the reported mean change because endpoint analyses may use different available-patient populations or model-based estimates. The two numbers should therefore not be forced into a simple subtraction equation. The most important correction to circulating coverage is this: > 24.53 millimeters of mercury was the baseline unmedicated pressure, not the 24-month pressure. The reported 24-month mean pressure was 16.76 millimeters of mercury. The original paper is the appropriate source for these values. () How durable was the medication-free result? At approximately month 23, 82.0% of patients were reported to be medication-free. That is a strong result, but it should be interpreted carefully. “Medication-free” does not mean that the glaucoma was cured. It means that, at that point in follow-up, the patient was not using pressur Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/a-glaucoma-laser-treatment-lowered-eye-pressure-for-4-years-without-cutting-into-the-eye Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: A Glaucoma Laser Treatment Lowered Eye Pressure for 4 Years Without Cutting Into the Eye Evidence review current to September 21, 2026 Bottom line The newest 48-month results for femtosecond laser image-guided high-precision trabeculotomy, called FLigHT, are encouraging but still preliminary. In the original first-in-human cohort: 18 eyes from 12 patients were treated. 15 eyes remained evaluable at 48 months. Mean medicated intraocular pressure decreased from 21.4 ± 4.6 millimeters of mercury to 14.9 ± 2.6 millimeters of mercury. That is approximately a 27% reduction, or about 6.5 millimeters of mercury. Mean glaucoma medication use decreased only modestly, from 2.1 to 1.8 medications, and the reduction was not statistically significant. The study did not use medication washout. The treated channels reportedly remained visible and patent on gonioscopy and anterior-segment optical coherence tomography after four years. No serious FLigHT-related adverse events were reported in the available 48-month reports. The key qualification is that this was a small, single-center, nonrandomized, single-arm study without a control group. The 48-month data have been presented at the European Society of Cataract and Refractive Surgeons meeting, but a complete peer-reviewed 48-month publication was not available in the public sources reviewed. My assessment is: > FLigHT has shown a credible four-year durability signal and pressure lowering in the general range of trabecular minimally invasive glaucoma surgery. It has not yet demonstrated that it is better than selective laser trabeculoplasty, equivalent to established minimally invasive glaucoma surgery, or reliably medication-sparing. The most likely future role is not replacing every glaucoma procedure. It is becoming a treatment option between selective laser trabeculoplasty and incisional minimally invasive glaucoma surgery, particularly for patients with open-angle glaucoma who need pressures in the low-to-mid teens but do not yet require the very low pressures often sought with trabeculectomy. --- What was newly reported at the 2026 European Society of Cataract and Refractive Surgeons meeting? The 44th European Society of Cataract and Refractive Surgeons Congress was held in London from September 11 through September 15, 2026. The 48-month FLigHT update was presented by Zoltan Nagy and colleagues as ePoster POGAU064. Ophthalmology Times conference report Media MICE conference report () The 48-month results For the full table, please open this article on visualfieldtest.com. The pressure reduction was statistically significant, with a reported P value below .001. However, the available conference reports do not provide the full patient-level dataset, confidence intervals, individual pressure trajectories, or a complete breakdown of medication classes. How many patients were still being followed? The publicly described 48-month result is based on 15 of the original 18 treated eyes, which represents an eye-level retention of approximately 83%. The accessible reports do not clearly identify: How many individual patients those 15 eyes represented The exact reason each missing eye was not included Whether missing eyes were lost to follow-up, had incomplete testing, or were excluded for another reason Therefore, the most defensible statement is: > Three of 18 treated eyes were not included in the 48-month analysis. Patient-level attrition is not fully reported in the public conference coverage. This matters because small studies can look better when participants with less favorable results are disproportionately lost from follow-up. --- What was the original first-in-human study? The first human study was a: Prospective Nonrandomized Single-center Single-arm Interventional safety study It was performed at Semmelweis University in Budapest, Hungary, with treatment performed in September and October 2020. The study was registered as NCT04949802. ClinicalTrials.gov study record Nagy et al., 24-month primary report () Patients and glaucoma severity The cohort included 18 eyes from 12 patients with open-angle glaucoma. The later three-year conference report described the group as: Approximately 33% mild glaucoma Approximately 28% moderate glaucoma Approximately 39% severe glaucoma Mean age: 72.2 ± 9.7 years Approximately 92% female Approximately 89% pseudophakic, meaning they had already undergone cataract surgery The cohort was small and demographically narrow. All participants were reported to be Caucasian. This limits how confidently the results can be generalized to younger patients, different ethnic groups, angle anatomy variations, or patients with secondary forms of glaucoma. European Glaucoma Society 2024 abstract book () The original study excluded eyes with previous glaucoma procedures, including: Selective laser trabeculoplasty Glaucoma implants Previous glaucoma surgery Eye conditions that would prevent adequate visualization of the trabecular meshwork This means the first-in-human results primarily describe untreated trabecular anatomy, apart from ongoing glaucoma medications. Baseline pressure and medications For the longer-term cohort, baseline mean intraocular pressure was: 21.4 ± 4.6 millimeters of mercury Patients were using: 2.1 ± 1.0 glaucoma medications at baseline The published 24-month report used a slightly different analytic sample and reported a baseline pressure of approximately 22.3 millimeters of mercury, falling to 14.5 millimeters of mercury at 24 months. Mean medication use decreased from approximately 2.2 to 2.0 medications, a change that was not statistically significant. Nagy et al., 24-month primary report () --- Exactly how does FLigHT work? FLigHT is best understood as a laser-created trabeculotomy performed through an intact cornea. The ViaLuxe system combines: High-resolution gonioscopic imaging Optical coherence tomography imaging Computer-controlled femtosecond laser delivery The system identifies the trabecular meshwork and Schlemm’s canal. It then focuses femtosecond laser pulses into the drainage tissue. What was created in the first human study? Each treated eye received one channel in the nasal angle. The reported dimensions were approximately: 500 micrometers wide 200 micrometers high Approximately 400 micrometers deep in the later technical description The treatment used approximately 400 femtosecond pulses at a wavelength of 1080 nanometers. The channel crossed the trabecular meshwork and entered Schlemm’s canal. The first human channel treated only about 5 degrees of the angle. European Glaucoma Society 2024 abstract book Nagy et al., 24-month primary report () Is the anterior chamber entered? There are two different meanings of “entering the eye.” No surgical instrument enters the anterior chamber The procedure does not require: A corneal incision A paracentesis A surgical blade A cannula A goniotomy blade An implant The femtosecond laser is focused through the intact cornea. In that sense, the eye is not surgically opened. But the laser creates a channel that communicates with the anterior chamber The intended channel begins at the anterior-chamber side of the trabecular meshwork and crosses into Schlemm’s canal. Therefore, FLigHT is not biologically “non-penetrating.” It creates a real internal opening through the trabecular tissue. The more precise description is: > FLigHT is externally incision-free but internally channel-forming. That distinction is important. Calling it “noninvasive” describes the absence of an external incision; it does not mean that the trabecular tissue is left intact. Anesthesia and preparation In the original first-in-human protocol: Topical anesthetic eye drops were used. Pilocarpine 2% was administered approximately one hour before treatment to constrict the pupil. Oral acetazolamide, 250 milligrams, was given two hours before treatment as a precaution against an early pressure spike. A specialized coupling lens and gonioscopic interface were placed on the cornea. The acetazolamide was a precaution used in the first human cases and should not automatically be assumed to be required for every commercial treatment. How long does treatment take? The first published study did not provide a clear standardized treatment-time measurement. Reports from the first commercial cases describe approximately two to three minutes of laser treatment per eye, with some clinic reports describing the complete procedure as approximately five minutes. The Ophthalmologist clinical report () This is considerably shorter than most operating-room-based glaucoma procedures, although total visit time includes preparation, imaging, docking, verification, and post-treatment assessment. Can it be repeated? The ViaLuxe system is designed to allow: More than one channel Customized channel placement Treatment in additional areas of the angle Retreatment if pressure later rises However, this is an important distinction: > Retreatment is a technical possibility, not yet a clinically validated long-term strategy. The first-in-human cohort received one channel per eye. There is not yet strong clinical evidence showing how much additional pressure lowering is obtained by creating a second or third c Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/can-we-improve-fluid-absorption-around-a-trabeculectomy-bleb-evidence-lymphatic-drainage-and-plausible-ways-to-reduce-discomfort Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Can We Improve Fluid Absorption Around a Trabeculectomy Bleb? Evidence, Lymphatic Drainage, and Plausible Ways to Reduce Discomfort Literature reviewed through September 16, 2026. Introduction A trabeculectomy intentionally creates a new pathway for aqueous humor to leave the eye. The fluid passes through the scleral flap and collects beneath the conjunctiva, creating a filtering bleb. The bleb is not simply a passive “bubble.” It is a reservoir connected to surrounding conjunctival tissue, lymphatic vessels, blood vessels, and the deeper orbital tissues. For a person with a functioning trabeculectomy and a previously measured intraocular pressure around 7 millimeters of mercury, the key question is: > Can fluid already present outside the eye be cleared more efficiently so the bleb becomes less raised or uncomfortable, without increasing flow through the surgical opening or causing a clinically important pressure reduction? The answer is biologically plausible but clinically unproven. The strongest modern evidence indicates that conjunctival lymphatic vessels are a genuine downstream drainage route from subconjunctival blebs. However, deliberately increasing lymphatic drainage could also reduce resistance downstream, increase total filtration, and lower intraocular pressure further. This is particularly relevant when the pressure is already low. For many patients, discomfort from a functioning bleb is caused less by failure to absorb fluid and more by: the shape or location of the bleb; eyelid friction during blinking; disruption of the tear film; a small corneal epithelial defect or corneal dellen; surrounding conjunctival swelling; inflammation; or clinically significant hypotony. Therefore, the most rational approach is to separate three goals: Reduce ocular-surface discomfort without changing filtration. Correct an abnormal bleb shape while preserving as much filtration as possible. Investigate downstream lymphatic clearance as a future treatment target, rather than attempting to stimulate it independently at home. --- The Complete Fluid Pathway The pathway in simple terms Step 1: Production in the eye Aqueous humor is produced by the ciliary body and enters the anterior chamber. In an untreated eye, most aqueous humor leaves through the trabecular meshwork and Schlemm canal. Trabeculectomy bypasses much of this conventional resistance. Step 2: Passage through the surgical opening A trabeculectomy creates a controlled route through the sclera. Fluid may pass: beneath the scleral flap; around the edges of the flap; through the sclerostomy; and through adjacent scleral or connective tissue planes. The scleral flap, its sutures, the size of the opening, and postoperative scarring determine much of the resistance before fluid reaches the bleb. This is the important distinction in the question: improving downstream clearance would not necessarily enlarge the internal opening, but it could reduce pressure behind the flap and thereby alter the pressure gradient across it. Step 3: Distribution within the bleb Once outside the eye, aqueous humor may occupy: a relatively large fluid-filled cavity; multiple smaller cavities; microcysts within the bleb wall; loose connective-tissue spaces; or a combination of these. Anterior segment optical coherence tomography studies have shown that functioning blebs may contain multiple internal layers, microcysts, and fluid-filled cavities. Larger internal fluid spaces and greater bleb dimensions are often associated with lower postoperative pressure, although appearance alone does not reliably predict pressure or comfort. () A raised bleb therefore does not automatically mean that fluid is “trapped” abnormally. Some elevation is the visible expression of successful filtration. Step 4: Clearance from the subconjunctival tissues There are several possible downstream routes. Route A: Conjunctival lymphatic drainage This is now the most strongly supported organized drainage route. The conjunctiva contains a rich lymphatic network. Experimental studies have shown that fluid injected into the subconjunctival space can enter irregular, sausage-shaped channels containing valve-like structures. These pathways express lymphatic markers such as podoplanin and Prospero-related homeobox 1, but do not match the pattern of ordinary blood vessels. () A 2019 prospective cross-sectional human study examined 13 eyes after trabeculectomy. Trypan blue injected into the anterior chamber stained lymphatic structures in eight eyes. Those eyes had a mean intraocular pressure of 12.6 millimeters of mercury, compared with 23.6 millimeters of mercury in the five eyes without visible lymphatic staining. Greater lymphatic extent was associated with lower pressure. This supports a functional relationship, but the study was small and observational. () A 2021 live-human imaging study found valve-containing intraconjunctival pathways after subconjunctival tracer injection. In the timed group, visible pathways appeared in seven of ten eyes after approximately 16 minutes, whereas they were not visible immediately after injection. The findings support delayed movement into lymphatic-like pathways, although the participants generally had retinal disease and repeated ocular injections rather than uncomplicated, healthy conjunctiva. () The lymphatic route likely continues toward regional lymph nodes and then returns fluid to the venous circulation. A mouse study using quantum-dot tracers detected signal in the submandibular lymph node approximately six hours after ocular injection, providing direct evidence of an eye-to-lymph-node drainage route in that species. () Route B: Diffuse movement toward blood vessels Blood vessels may still absorb some fluid from the conjunctival tissue through ordinary interstitial and vascular exchange. However, they appear less likely to be the principal organized bulk-flow pathway from a filtering bleb. In porcine, bovine, and human postmortem eyes, tracer-filled subconjunctival outflow pathways were associated with lymphatic markers and did not co-localize with the blood-vessel marker CD31. These studies do not prove that blood vessels absorb no fluid; they show that the distinctive valve-containing pathways from blebs are more consistent with lymphatics than with blood vessels. () A reasonable mechanistic interpretation is: Lymphatics provide directed, low-pressure bulk drainage. Blood vessels may contribute to diffuse absorption from the surrounding tissue. The relative contribution probably varies with bleb structure, inflammation, scarring, and local vascularity. Route C: Diffuse movement through tissue planes Fluid may spread through the conjunctival stroma and Tenon tissue before entering lymphatic or vascular channels. This is not a separate “drain” so much as the tissue pathway leading to the drains. Fibrosis, a dense extracellular matrix, local tissue compression, and isolated fluid pockets can all increase resistance to movement through these planes. Route D: Evaporation through the ocular surface Evaporation from the tear film is not a credible major route for clearing aqueous humor from a functioning bleb. It may influence superficial surface moisture, but it cannot reasonably account for sustained aqueous filtration from the eye. This is a mechanistic inference from the continuous volume of aqueous humor entering the bleb and the observed lymphatic outflow pathways. () --- What Limits Downstream Clearance? Downstream clearance can be limited at several different levels. A. Few or poorly connected lymphatic vessels The bleb may have limited access to nearby lymphatic channels. Human post-trabeculectomy studies suggest that lymphatic connections are variable: some blebs show obvious connections while others do not. () B. Scar tissue and altered extracellular matrix Fibrosis can: isolate the bleb from surrounding lymphatics; compress small lymphatic channels; create a thick capsule around a fluid pocket; reduce tissue compliance; and force fluid to collect in a narrow, high-pressure compartment. C. Antimetabolite-related lymphatic suppression Mitomycin C and 5-fluorouracil are used to reduce fibroblast proliferation and scarring after glaucoma surgery. Animal studies suggest that these drugs can also reduce subconjunctival lymphatic branching and length. In mouse eyes, mitomycin C and 5-fluorouracil reduced lymphatic presence in some experimental protocols, whereas vascular endothelial growth factor C increased it. () This creates an important biological tradeoff: > The same tissue-modifying strategy that helps preserve a filtering bleb by reducing scar formation may also reduce the lymphatic network available to clear fluid from it. That does not mean mitomycin C was a mistake or that it should be reversed. It means that fibrosis control and lymphatic preservation are separate biological objectives. D. Downstream venous or lymphatic pressure Lymphatic drainage is not determined only by the number of vessels. Flow also depends on: tissue pressure; lymphatic valve function; contraction of collecting lymphatics; pressure in downstream lymphatic channels; nea Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/could-glaucoma-surgery-become-a-10-minute-office-procedure-first-human-results-from-obi-core Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Could Glaucoma Surgery Become a 10-Minute Office Procedure? First Human Results From OBi Core Short answer: OBi Core is one of the more interesting new glaucoma procedures because it attempts to combine the pressure-lowering power of filtration surgery with the convenience of an office-based slit-lamp procedure. But the current evidence is still extremely early. The publicly reported human experience consists of a small first-in-human series of approximately 10 eyes with detailed results, followed by a company update describing 11 treated eyes. Follow-up is short, patient-level data are not publicly available, and approximately 30% of eyes required reintervention in the initial detailed report. () The technology is therefore promising, but not yet proven to replace trabeculectomy. Its most important scientific question is not whether it can lower pressure initially. The early data suggest that it can. The difficult question is whether the subconjunctival bleb can remain functional for years without recreating the fibrosis, needling, medication, and monitoring burden of conventional filtering surgery. The Bottom Line OBi Core is not a conventional angle-based minimally invasive glaucoma surgery. It creates a direct pathway from the anterior chamber to a subconjunctival or sub-Tenon filtration space. The device appears to use a 27-gauge, 6-millimeter punch needle to create an oblique scleral microchannel approximately 150 ± 50 micrometers in diameter. () It does create a subconjunctival filtration bleb, meaning it shares the central biological weakness of trabeculectomy, XEN Gel Stent, and PreserFlo MicroShunt: wound healing and fibrosis can eventually reduce flow. The detailed first-in-human report involved 10 eyes followed for up to approximately 6 weeks. Mean intraocular pressure fell from 30.1 to 10.2 millimeters of mercury, a calculated absolute reduction of 19.9 millimeters of mercury, or approximately 66%. Mean glaucoma medications fell from 2.2 to 0.8, an absolute reduction of 1.4 medications, or approximately 64%. Seventy percent of eyes reportedly achieved complete success under the study definition, and approximately 78% were medication-free, although the denominators and patient-level data were not fully disclosed. Thirty percent required reintervention, including repeat OBi Core procedures or other filtration procedures. The reasons for those interventions have not been publicly separated into fibrosis, obstruction, inadequate flow, or surgical learning-curve effects. () A September 2026 company update described 11 treated eyes, including mild, moderate, and advanced glaucoma, with early pressures in the single digits to low teens and no reported device- or procedure-related adverse events. No detailed aggregate results from the eleventh eye were provided. () The “10-minute” description is not yet supported by a published procedural-time dataset. The channel-creation step may take seconds, but the full visit—including preparation, anesthesia, mitomycin C, intraocular pressure management, and postoperative testing—has not been formally reported. What Is OBi Core? Manufacturer and development status OBi Core is being developed by Hexiris Ophthalmics, a Canadian company based in Dieppe, New Brunswick. Hexiris describes OBi Core as a device for minimally invasive bleb surgery, usable either at the slit lamp or in an operating room. () The clinical-trial registry uses the more generic name Hexiris Microinvasive Scleral Trephine, or MIST. The registered first-in-human study is a Canadian, multicenter, open-label, single-arm study intended to enroll 25 adults with primary open-angle glaucoma. The first five cases are planned in an operating room, after which the safety monitor may allow the remaining procedures to move to an aseptic slit-lamp setting. () Hexiris states that OBi Core has a Health Canada medical device license and is FDA registered. FDA registration does not by itself mean that a device has received United States clearance or approval for routine commercial use. The company has indicated that commercial introduction in selected markets may begin in early 2027, subject to regulatory requirements. () Device design The publicly described OBi Core system consists of: A handpiece A 27-gauge punch needle A needle approximately 6 millimeters long An actuator that advances the cutting element A scleral punch that removes a small core of tissue A resulting oblique microchannel approximately 150 ± 50 micrometers in diameter The device is not described as leaving a permanent implant in place. Instead, it creates a tissue channel. A related Hexiris patent describes the concept as a drainage pathway created by removing a small tissue core, with no artificial tube left inside that channel. () That is an important distinction: XEN and PreserFlo leave a permanent implant. OBi Core appears to create a micro-sclerostomy without leaving a permanent tube. A separate Hexiris product called OBi Shunt is being developed as an implantable device, but it is a different product and should not be confused with OBi Core. () What Drainage Pathway Does It Create? The publicly described pathway is: > Anterior chamber → scleral microtunnel → posterior subconjunctival or sub-Tenon space → absorption through surrounding tissues and episcleral vessels The approach is ab externo, meaning the surgeon approaches the eye from the outside. The device is placed through the conjunctiva and sclera, with the punch directed into the anterior chamber. The described target location is generally the superior or superotemporal sclera, approximately 1.0 to 1.5 millimeters behind the limbus. () The procedure is therefore a form of penetrating filtration surgery, although it is much smaller than a traditional trabeculectomy. Is a bleb formed? Yes. OBi Core is a bleb-forming procedure. Aqueous humor is intended to collect in a posterior subconjunctival or sub-Tenon space, creating a filtration reservoir. This reservoir is commonly called a bleb. The fluid is then absorbed through surrounding tissue and blood vessels. () This means OBi Core does not completely escape the biological problems of conventional glaucoma filtration surgery. It may reduce tissue trauma, but it still depends on: A functioning drainage channel A healthy subconjunctival space Controlled wound healing A bleb that remains open rather than becoming scarred or encapsulated How Is the Procedure Performed? The exact first-in-human operative protocol has not been published in a peer-reviewed clinical paper. However, the publicly described technique includes the following elements. Publicly described procedural sequence The eye is anesthetized with topical anesthesia. The procedure is performed at the slit lamp in an aseptic office environment. A small subconjunctival or sub-Tenon pocket is created or accessed. A bolus of cohesive ophthalmic viscoelastic is placed in the anterior chamber to reduce excessive early flow. The OBi Core device is positioned on the superior or superotemporal sclera. The actuator advances the punch needle through the conjunctiva and sclera into the anterior chamber. A small scleral tissue core is removed, creating the microchannel. Mitomycin C is injected into the subconjunctival pocket. Pilocarpine may be used to pull the iris away from the internal opening. The surgeon performs a Seidel test to look for leakage. Postoperative antibiotics and steroids are prescribed. The bleb and intraocular pressure are monitored closely. The described technique includes mitomycin C at 0.4 milligrams per milliliter, equivalent to approximately 0.04%. The registered MIST trial specifies a subconjunctival mitomycin C concentration of 0.02% to 0.04%. () Is it performed entirely at a slit lamp? The intended office-based version appears to be performed at the slit lamp, without major capital equipment. However: The first five cases in the registered study are planned in an operating room. The procedure can also be performed in an operating room. The surgeon must still enter the anterior chamber. The eye must be prepared with sterile or aseptic technique. The practice must be capable of recognizing and managing hypotony, bleeding, iris obstruction, wound leakage, and other intraocular problems. Thus, “office-based” does not mean “noninvasive” or “risk-free.” How long does it take? The available clinical sources call the procedure rapid, and the underlying patent describes the tissue-channel creation step as occurring in the order of seconds. However, no reliable published study currently reports the total procedure time from patient preparation to discharge. () The most accurate conclusion is: > OBi Core may be a short office procedure, but the public evidence does not yet establish that the complete treatment reliably takes 10 minutes. The full time would include topical anesthesia, sterile preparation, conjunctival manipulation, anterior chamber viscoelastic, mitomycin C injection, pressure testing, and postoperative instructions. Reconstructing the First Human Results Detailed first-in-human report The most detailed publicly available report came from a presentation at the 2026 American Society of Cataract and Refractive Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/can-high-dose-vitamin-b3-protect-the-optic-nerve-a-new-glaucoma-trial-will-test-3-grams-a-day Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Can High-Dose Vitamin B3 Protect the Optic Nerve? A New Glaucoma Trial Will Test 3 Grams a Day Research updated September 13, 2026 Introduction Glaucoma treatment has traditionally focused on one target: lowering intraocular pressure. That strategy clearly helps, but it does not eliminate risk. Some patients continue to lose retinal ganglion cells and visual-field sensitivity even when their eye pressure appears well controlled. The NADIR trial—NCT07808333—is designed to test a different strategy. It will add high-dose oral nicotinamide, the non-flushing form of vitamin B3, to standard glaucoma treatment and measure whether the inner retinal layers thin more slowly. The central biological idea is straightforward: > Retinal ganglion cells may become metabolically fragile before they die. If nicotinamide raises cellular nicotinamide adenine dinucleotide availability, it might help stressed but living cells withstand glaucoma-related injury. That hypothesis is supported by striking animal research, early human electrophysiology studies, and a plausible link between aging, mitochondrial dysfunction, impaired axonal transport, and retinal ganglion-cell degeneration. But the human evidence remains preliminary—and 3 grams daily is a pharmacological dose, not an ordinary nutritional supplement dose. My overall assessment is that nicotinamide is one of the most credible current candidates for pressure-independent glaucoma neuroprotection, but it is not yet proven to slow glaucoma progression in humans. --- The NADIR Trial: What Is Actually Being Tested? As of September 13, 2026, NADIR is listed as not yet recruiting. It is a single-center University of Chicago study expected to begin enrollment in June 2027. The registry describes it as a Phase 2 study, while the protocol title calls it a Phase 2a trial. () Trial summary For the full table, please open this article on visualfieldtest.com. The trial is important because it is not asking whether nicotinamide lowers eye pressure. It is asking whether it protects retinal tissue despite ongoing standard pressure-lowering treatment. Who can participate? NADIR is designed for adults with mild to moderate primary open-angle glaucoma, not advanced disease. Key inclusion requirements include: Age 40 to 80 years Primary open-angle glaucoma in at least one eye Study-eye visual-field mean deviation between −2.0 and −12.0 decibels At least one reliable Humphrey 24-2 visual-field test Fixation losses of 33% or less False-positive responses of 15% or less Best-corrected visual acuity of 20/40 or better Structural damage on optical coherence tomography and/or a reproducible glaucomatous visual-field defect Macular ganglion cell-inner plexiform layer and retinal nerve fiber layer thickness above the device’s measurement floor Stable pressure-lowering therapy for at least four months Screening intraocular pressure of 21 millimeters of mercury or less The visual-field range is strategically chosen. Patients with mean deviation between −2 and −12 decibels still have enough surviving retinal tissue for a protective treatment to be measurable, but they have established disease rather than merely being glaucoma suspects. () Who is excluded? The important exclusions include: Advanced glaucoma with mean deviation worse than −12 decibels Best-corrected visual acuity worse than 20/40 Significant retinal disease, including advanced age-related macular degeneration or more than mild diabetic retinopathy Non-glaucomatous optic neuropathy Recent eye surgery Liver dysfunction, including alanine aminotransferase or aspartate aminotransferase greater than twice the upper limit of normal Total bilirubin greater than 1.5 times the upper limit of normal Estimated glomerular filtration rate below 30 milliliters per minute per 1.73 square meters Poorly controlled diabetes, defined as hemoglobin A1c greater than 9% Current use of nicotinamide, high-dose vitamin B3, nicotinamide adenine dinucleotide supplements, gingko biloba, coenzyme Q10, or certain drugs that could complicate safety interpretation Pregnancy or breastfeeding Active ocular inflammation Media opacity that prevents reliable imaging Patients with untreated normal-tension glaucoma are also excluded. NADIR is therefore testing an adjunctive treatment in patients whose glaucoma is being treated conventionally, not a therapy for every glaucoma subtype. () Nicotinamide dosing: Why 1.5 grams, then 3 grams? Participants assigned to the treatment arm will take: Weeks 1–6: 500 milligrams three times daily, totaling 1.5 grams daily Week 7 through month 12: 1,500 milligrams twice daily, totaling 3 grams daily The tablets are taken with meals. Advancement to the full dose requires an early safety review confirming acceptable gastrointestinal tolerance and no significant hepatic adverse event. () What is the basis for the escalation? The publicly available record does not describe a formal human exposure-response pharmacokinetic model. The dose appears to come from three sources: The earlier Australian human glaucoma study, which used 1.5 grams daily for six weeks followed by 3 grams daily for six weeks. Mouse glaucoma studies, in which relatively high nicotinamide exposure produced the strongest protection. A mechanistic assumption that substantial nicotinamide availability may be needed to overcome age-related or disease-related limitations in the nicotinamide adenine dinucleotide salvage pathway. The 3-gram dose was not selected because it is a standard nutritional requirement. The recommended daily amount of vitamin B3 is roughly 14–16 milligrams in adults, making 3 grams approximately 150 to 200 times the usual nutritional intake. Animal investigators have described 3 grams daily as the lowest human-equivalent dose likely to reproduce the effective exposure seen in their mouse model. A later rat study used doses equivalent to approximately 2.1 grams and 6.3 grams daily in a 70-kilogram adult, with the higher dose needed for some intervention settings. This is body-surface-area extrapolation, not proof that humans require the same exposure. () NADIR’s endpoints Primary endpoint The primary outcome is the annualized rate of macular ganglion cell-inner plexiform layer thinning. Measurements will occur at: Baseline Month 3 Month 6 Month 12 The statistical analysis will use a linear mixed-effects model with: A participant-level random intercept Repeated measurements over time A treatment-arm-by-time interaction The key question is whether the nicotinamide group has a less negative slope than the standard-care group. Secondary structural and functional endpoints The secondary outcomes include: Annualized rate of peripapillary retinal nerve fiber layer thinning Visual-field mean deviation slope Grade 2 or higher hepatic and gastrointestinal adverse events Nicotinamide adherence Study retention Additional exploratory measures include: Macular superficial capillary plexus perfusion density by optical coherence tomography angiography Peripapillary radial capillary plexus perfusion density The registry specifies that optical coherence tomography and visual-field readers will be masked to treatment assignment through de-identified participant identifiers, even though participants and investigators will know which treatment is being given. () Statistical strengths and weaknesses Strengths Randomized 1:1 allocation Active standard-care control Stratification by mild versus moderate disease Stratification by race and ethnicity Masked structural and visual-field reading Repeated optical coherence tomography measurements A structural primary endpoint that may be more sensitive than visual-field change over only one year Weaknesses The trial is open-label There is no placebo Only 96 participants are planned It is being conducted at one center Twelve months is short for proving long-term visual-field preservation The public registry does not provide a detailed power calculation or a prespecified minimum clinically important difference A positive NADIR result would therefore be important, but it would probably be considered proof of biological activity, not definitive proof that nicotinamide should immediately become routine treatment. --- Why Might NAD Matter in Glaucoma? Nicotinamide adenine dinucleotide is an energy and repair molecule Nicotinamide adenine dinucleotide is needed for: Mitochondrial energy production Transfer of electrons during cellular respiration Maintenance of redox balance DNA repair Regulation of protein acetylation through sirtuin enzymes Calcium handling Axonal transport Cellular responses to oxidative stress Retinal ganglion cells are unusually vulnerable to energy failure. They have long axons, high electrical activity, substantial transport demands, and a portion of their axons that remain unmyelinated inside the retina. Their energy supply must remain reliable even when pressure-related mechanical stress affects the optic nerve head. Mitochondrial dysfunction may occur before obvious cell loss In the DBA/2J mouse model of glaucoma, abnormal mitochondrial gene expression, mitochondrial cristae disruption, oxidative phosphorylation changes, synapse loss, and pattern electroretinogram abnormalit Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/four-new-glaucoma-developments-from-the-last-two-weeks-which-one-could-matter-most-for-patients Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Four New Glaucoma Developments From the Last Two Weeks — Which One Could Matter Most for Patients? Between August 21 and September 4, 2026, four glaucoma developments attracted attention: G01 / rhNGF-V2 neuroprotective eye drops Acid sphingomyelinase and ceramide metabolism as retinal ganglion-cell targets Optical coherence tomography angiography for earlier progression detection NCX 470, now called K-911, approaching United States regulatory review They are not equally important. One is already available as a diagnostic technology. One is close to possible approval but appears to be an incremental pressure-lowering improvement. The other two could eventually change the biology of glaucoma, but both remain uncertain and relatively early. This assessment uses information available through September 4, 2026, with the current regulatory status checked through September 11, 2026. > Important: The probabilities below are informed estimates, not clinical-trial results or regulatory predictions. “Changing care” means becoming sufficiently useful that it changes routine glaucoma management within approximately the next 5–10 years. At-a-Glance Comparison For the full table, please open this article on visualfieldtest.com. The Short Answer Most likely to help patients in the next 5–10 years NCX 470 / K-911 is the most likely to produce a measurable patient benefit because it has already completed large Phase 3 trials and has entered regulatory review. Most likely to improve glaucoma monitoring Optical coherence tomography angiography is the most immediately useful development. It may identify progression roughly two years before visual-field progression in some patients, although it is not perfect and does not directly treat glaucoma. () Highest upside G01 / rhNGF-V2 has the greatest potential upside because it aims to protect retinal ganglion cells independently of intraocular pressure. However, its current evidence is much weaker than the evidence supporting NCX 470. Most interesting biological discovery The acid sphingomyelinase–ceramide pathway may reveal a new way to protect retinal ganglion cells, but it is still a target rather than a treatment. --- G01 / rhNGF-V2 Neuroprotective Eye Drops What was reported? G01 is an investigational eye drop being developed in China for optic nerve injury associated with open-angle glaucoma. A Phase 2 study was updated on August 24, 2026, after being first posted on August 20, just outside the requested date range. The randomized, double-masked study plans to enroll approximately 90 patients with progressing primary open-angle glaucoma. It compares G01 concentrations of 100 micrograms per milliliter and 200 micrograms per milliliter with placebo. The study’s primary outcome is change in visual-field mean deviation after approximately 24 weeks of treatment, with additional structural, electrophysiological, pharmacokinetic, and immunogenicity measurements. Completion is estimated for late 2027. () A separate Phase 1 study in healthy volunteers is testing single and repeated doses of 100, 200, and 400 micrograms per milliliter. No public clinical efficacy results were available by September 4, 2026. () What is rhNGF-V2 supposed to do? Nerve growth factor is a neurotrophic protein involved in neuronal survival and repair. The goal is not to lower eye pressure but to make retinal ganglion cells more resistant to injury. Public company information identifies G01’s active ingredient as recombinant human nerve growth factor variant 2. A related patent describes a modified nerve growth factor known as K34D, which appears to be the likely molecular identity of rhNGF-V2, although the exact identity and characteristics of the clinical product have not been independently confirmed in a peer-reviewed clinical publication. This is therefore a strong inference, not a fully established fact. () The proposed advantage of the modified molecule is greater signaling through the protective tropomyosin receptor kinase A pathway with less potentially harmful signaling through the p75 neurotrophin receptor. The patent reports substantially reduced binding to the p75 receptor for K34D and even more receptor selectivity for a related double-mutant molecule. () Strength of the evidence Known facts G01 is in a registered Phase 2 glaucoma trial. No G01 efficacy results have been publicly reported. A separate healthy-volunteer safety and pharmacokinetic study is also registered. A patent reports protective effects for K34D in rat ocular-hypertension models. Earlier human research with conventional recombinant human nerve growth factor established short-term safety but did not demonstrate statistically significant neuroenhancement. Animal evidence In a patent-described rat model of chronic ocular hypertension, treatment began after pressure elevation had already occurred. K34D eye drops did not lower intraocular pressure, but they were associated with: Less retinal ganglion-cell loss Less optic-nerve axon damage Better pattern electroretinogram responses In one experiment, retinal ganglion-cell loss was approximately 59% in vehicle-treated animals versus 31% with K34D, a roughly 50% relative reduction in cell loss. However, the groups were small, the work was reported in a patent rather than an independent peer-reviewed paper, and the findings have not yet been replicated publicly by unrelated laboratories. () Human evidence for the nerve growth factor class A Phase 1b randomized trial gave conventional recombinant human nerve growth factor to 40 patients and vehicle to 20 patients for eight weeks. It found: No treatment-related serious adverse events No meaningful intraocular-pressure effect No statistically significant short-term improvement in visual fields or optical coherence tomography Ocular pain in approximately half of the nerve-growth-factor group Irritation, photophobia, and other surface symptoms in some patients The researchers noted that the trial was too short and too small to test true neuroprotection. Still, the absence of a clear short-term functional signal is important. It means that the modified G01 molecule must prove that it is meaningfully better than conventional nerve growth factor, not merely safer or more selective. () Biological plausibility The biological rationale is strong enough to justify clinical testing: Retinal ganglion cells depend on neurotrophic support. Glaucoma involves axonal injury, impaired transport, metabolic stress, and eventual cell death. Neurotrophic signaling could theoretically preserve stressed but living retinal ganglion cells. The patent data suggest a possible advantage from modifying receptor selectivity. The main biological problem is delivery. A topical eye drop must reach the retina and optic nerve in an adequate concentration. The cornea, anterior chamber, lens, vitreous, and retinal barriers make posterior-segment delivery difficult. A large dose may be needed, which could worsen surface pain or irritation. Potential magnitude of benefit Maximum plausible benefit If the animal findings translate unusually well to humans, G01 could: Slow retinal ganglion-cell death by a substantial amount Delay visual-field progression Provide benefit even when intraocular pressure is already at target Possibly improve function in retinal ganglion cells that are impaired but not yet dead Most realistic benefit The more realistic initial outcome would be a modest slowing of progression, perhaps in a subgroup of patients with active disease despite acceptable intraocular pressure. A benefit of approximately 10–25% slower functional deterioration would be clinically useful but would not constitute a cure. The possibility of a 30–50% reduction in progression is biologically conceivable but currently speculative. Risks The major known concern is tolerability. Conventional nerve growth factor produced substantial ocular pain and irritation in the Phase 1b trial. A modified molecule may have a better profile, but this has not yet been demonstrated in patients. Other concerns include: Ocular surface inflammation Photophobia and discomfort Immunogenicity against a repeated protein treatment Insufficient retinal exposure Possible unintended effects on sensory nerves or inflammatory signaling The need for multiple daily doses Likely patient population The most likely initial target would be patients with: Progressing open-angle glaucoma Intraocular pressure already reasonably controlled Mild-to-moderate disease with surviving retinal ganglion cells Documented structural or visual-field progression Patients with advanced glaucoma could benefit from preservation of remaining vision, but a treatment cannot rescue retinal ganglion cells that have already died. Does it work independently of intraocular pressure? Probably yes. The patent experiments reported no intraocular-pressure lowering, yet showed retinal ganglion-cell and axon protection. The current Phase 2 trial also appears designed for patients with relatively controlled pressure, strengthening the idea that G01 is intended as an adjunctive, pressure-independent treatment. () Could it preserve or restore vision? Preserve vision: Potentially yes. Restore lost function: Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/a-new-glaucoma-drug-is-approaching-fda-approval-can-it-lower-eye-pressure-better-than-today-s-best-drops Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: A New Glaucoma Drug Is Approaching FDA Approval — Can It Lower Eye Pressure Better Than Today’s Best Drops? Evidence reviewed through September 10, 2026 Bottom line NCX 470—now called K-911, with the proposed generic name bimatoprost grenod—has been accepted for Food and Drug Administration review. The New Drug Application was submitted by Kowa on June 30, 2026, accepted for review on August 27, 2026, and assigned a Prescription Drug User Fee Act decision date of April 30, 2027. It is not yet approved. Kowa FDA acceptance announcement () The clinical evidence shows that NCX 470: Lowers intraocular pressure by approximately 8 to 10 millimeters of mercury in patients starting with pressures around 26 to 28 millimeters of mercury. Produces roughly 0.5 to 0.8 millimeters of mercury more reduction than latanoprost in the strongest published phase 3 dataset. Performs better than latanoprost at several individual time points, but the average advantage is modest rather than dramatic. Has more conjunctival hyperemia, or eye redness, than latanoprost. Has not been directly compared with bimatoprost, latanoprostene bunod, Rocklatan, or Cosopt in a pivotal head-to-head trial. Has not been adequately studied in patients starting with pressures in the mid-teens or in patients who need targets near 10 to 12 millimeters of mercury. My overall judgment: NCX 470 appears to be a meaningful incremental improvement over latanoprost, but not a breakthrough that is likely to replace combination therapy, selective laser trabeculoplasty, or glaucoma surgery. --- Current regulatory status For the full table, please open this article on visualfieldtest.com. FDA acceptance means the application was considered complete enough for formal review. It does not mean that approval is guaranteed. Kowa product pipeline Kowa FDA announcement () The application is supported principally by the MONT BLANC and DENALI phase 3 trials. A small phase 3b study called WHISTLER examined the drug’s effect on aqueous humor outflow but was exploratory and was not required for the New Drug Application. Nicox pre-New Drug Application update () --- What is NCX 470? NCX 470 is a nitric-oxide-donating version of bimatoprost. After the molecule is exposed to esterases in the eye, it releases: Bimatoprost-related prostaglandin activity, which primarily increases uveoscleral outflow. Nitric oxide, which is intended to relax the trabecular meshwork and improve drainage through the conventional trabecular meshwork–Schlemm canal pathway. In simplified terms: Bimatoprost helps fluid leave through the uveoscleral route. Nitric oxide attempts to improve the eye’s conventional drainage system. This is conceptually similar to latanoprostene bunod, marketed as Vyzulta, which combines a prostaglandin effect with nitric oxide donation. The difference is that Vyzulta releases a latanoprost-derived prostaglandin, whereas NCX 470 releases bimatoprost-related activity. NCX 470 mechanism and preclinical research MONT BLANC publication () --- The pivotal clinical trials MONT BLANC phase 3 trial The MONT BLANC study was a randomized, double-masked, multicenter phase 3 trial conducted at 56 United States sites and one site in China. A total of 691 patients were randomized. MONT BLANC publication ClinicalTrials.gov record () Treatment groups NCX 470 0.065%, once daily NCX 470 0.1%, once daily Latanoprost 0.005%, once daily The 0.065% arm included 30 initial patients and was stopped after the planned interim analysis. The final efficacy comparison involved: NCX 470 0.1%: 328 patients Latanoprost 0.005%: 333 patients The drops were administered to both eyes, generally in the evening. Baseline intraocular pressure The final treatment groups had very similar baseline values: For the full table, please open this article on visualfieldtest.com. These patients had relatively high baseline pressures. They were required to have untreated or washed-out pressure of at least approximately 26 millimeters of mercury at 8:00 a.m., 24 at 10:00 a.m., and 22 at 4:00 p.m. ClinicalTrials.gov results MONT BLANC responder analysis () Primary endpoint The primary endpoint was the reduction from time-matched baseline pressure at: 8:00 a.m. and 4:00 p.m. Week 2 Week 6 Month 3 The primary statistical goal was noninferiority to latanoprost. A secondary analysis examined whether NCX 470 was statistically superior. MONT BLANC: actual numerical results The table below uses the reported mean reductions from baseline. Percent reductions are calculated from the published baseline values. For the full table, please open this article on visualfieldtest.com. The reductions were statistically significant compared with baseline at every evaluated time point. NCX 470 was numerically better than latanoprost at all six time points and statistically better at four of them. ClinicalTrials.gov numerical results () Mean diurnal pressure results The secondary mean diurnal pressure analysis showed: For the full table, please open this article on visualfieldtest.com. This suggests that the average incremental benefit over latanoprost was approximately 0.5 to 0.8 millimeters of mercury, with an average across these visits of about 0.64 millimeters of mercury. That is a real difference. However, it is not the type of difference that usually transforms a patient from needing several medications to needing none. --- DENALI phase 3 trial DENALI was the second pivotal phase 3 trial. It randomized 696 patients at 90 sites in the United States and China: NCX 470 0.1%: 348 patients Latanoprost 0.005%: 348 patients Treatment was once daily in both eyes. All patients were followed through approximately six months, while a subset contributed safety data through 12 months. DENALI trial summary ClinicalTrials.gov DENALI record () Baseline pressure For the full table, please open this article on visualfieldtest.com. Reported efficacy Across the six prespecified efficacy time points: NCX 470 reduced pressure by 7.9 to 10.0 millimeters of mercury. Latanoprost reduced pressure by 7.1 to 9.8 millimeters of mercury. NCX 470 was numerically better at five of six time points. The difference favored NCX 470 by as much as 0.8 millimeters of mercury. Statistical superiority was demonstrated at three of six time points, but the overall superiority endpoint was not achieved. Thus, DENALI confirmed the general pattern seen in MONT BLANC: NCX 470 is at least as effective as latanoprost and sometimes modestly better, but the average advantage is not large. DENALI topline results () --- Comparison with other glaucoma medications Cross-trial comparisons must be interpreted cautiously. The studies used different entry pressures, populations, follow-up periods, statistical methods, and treatment schedules. A drug that appears stronger in one trial may have been tested in patients with higher starting pressure. Quantitative comparison For the full table, please open this article on visualfieldtest.com. Sources include the first-line glaucoma medication network meta-analysis, Vyzulta clinical review, ROCKET netarsudil trials, ROCKET-4, MERCURY Rocklatan pooled analysis, and fixed-combination medication meta-analysis. () NCX 470 versus latanoprost This is the best-established comparison. NCX 470 appears to provide: Approximately 0.5 to 0.8 millimeters of mercury more mean diurnal reduction in MONT BLANC. Approximately 0 to 0.8 millimeters of mercury more reduction in DENALI. A somewhat stronger morning effect, but the difference at 8:00 a.m. was inconsistent and small, ranging from 0.22 to 0.58 millimeters of mercury in MONT BLANC. The advantage is therefore statistically credible but clinically modest. NCX 470 versus bimatoprost This question is central because NCX 470 releases bimatoprost-related activity. NCX 470 has not been directly compared with marketed bimatoprost in a large pivotal human trial. A network meta-analysis of first-line drugs estimated that bimatoprost reduced pressure by approximately 5.61 millimeters of mercury, compared with 4.85 millimeters of mercury for latanoprost, a difference of approximately 0.76 millimeters of mercury. Network meta-analysis () That is important because the average NCX 470 advantage over latanoprost—roughly 0.5 to 0.8 millimeters of mercury—is similar in size to the historical advantage often reported for bimatoprost over latanoprost. Therefore, the pivotal trials do not prove that nitric oxide adds a large benefit beyond bimatoprost itself. Some of the observed difference may come from the bimatoprost component rather than the nitric oxide component. NCX 470 versus Vyzulta Vyzulta, or latanoprostene bunod, is the closest mechanistic competitor because it also combines a prostaglandin effect with nitric oxide donation. In the APOLLO and LUNAR trials: Mean baseline diurnal pressure was approximately 26.7 millimeters of mercury for latanoprostene bunod and 26.5 millimeters of mercury for timolol. Three-month mean pressure was approximately 17.8 millimeters of mercury with latanoprostene bunod and 19.1 millimeters of mercury with timolol. The implied reduction was approximately 8.9 millimeters of mercury with latanoprostene bunod, compared with approximat Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/a-new-scan-may-detect-glaucoma-progression-years-before-it-shows-up-on-a-visual-field-test Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: A New Scan May Detect Glaucoma Progression Years Before It Shows Up on a Visual Field Test Introduction A study published online on September 3, 2026, reported that optical coherence tomography angiography, or OCTA, detected event-based glaucoma progression an average of 2.3 years before visual-field progression. Conventional structural optical coherence tomography, or OCT, detected progression about 1.5 years before visual-field progression. JAMA Ophthalmology study () That sounds like a major breakthrough. It could imply that clinicians might identify worsening glaucoma long before patients lose measurable vision. However, the result needs careful interpretation. The study did not prove that OCTA detects the biological beginning of glaucoma damage two years earlier. It showed that an OCTA measurement crossed a predefined statistical threshold before a visual-field algorithm crossed its own threshold. Those are not necessarily the same thing. The most defensible conclusion is: > OCTA may provide an earlier vascular signal of progression in some eyes, but the evidence does not yet show that it reliably outperforms the best structural OCT strategy or that every OCTA alert represents irreversible retinal ganglion-cell loss. The New Study: What It Actually Found Study design and participants The study used patients from the Diagnostic Innovations in Glaucoma Study, a longitudinal research cohort. It included: 116 patients 180 eyes 111 eyes with perimetric glaucoma, meaning repeatable visual-field damage was already present 69 preperimetric eyes, meaning glaucomatous optic-nerve or structural damage was present without repeatable visual-field loss Mean age: 67.6 years Mean follow-up: 5.1 ± 1.4 years Minimum eligibility: at least 2 years of follow-up and at least four visits with each testing method The public abstract does not provide a detailed breakdown into mild, moderate, and advanced glaucoma. Therefore, it is not possible to know from the published abstract whether the two-year lead time was concentrated in early disease, moderate disease, advanced disease, or spread evenly across stages. JAMA Ophthalmology study () What was measured? The study compared: OCTA vessel-density change Circumpapillary retinal nerve fiber layer thickness change, measured by structural OCT Visual-field progression The abstract states that OCT and OCTA progression were defined as a change exceeding test-retest variability at two consecutive visits. Visual-field progression was assessed using the instrument’s Guided Progression Analysis. Important details are not available in the public abstract: The exact OCTA device The scan size Whether the main metric was peripapillary vessel density, optic-nerve-head vessel density, macular vessel density, or a combined measure The exact retinal slab The numerical test-retest thresholds Whether visual-field progression meant “possible” or “likely” Guided Progression Analysis progression Whether the structural OCT algorithm used only event analysis or also a slope-based trend analysis These missing details matter because OCTA vessel-density values are highly dependent on the device, scan size, software version, segmentation method, signal strength, and region measured. A related 2024 study from the same research group used an Optovue Avanti AngioVue system, with a 4.5-by-4.5-millimeter optic-nerve-head scan and a peripapillary annulus. But that study should not automatically be assumed to have used the identical protocol. Related event-based OCT/OCTA study () Progression detection During follow-up: For the full table, please open this article on visualfieldtest.com. Among the 107 eyes classified as progressing by at least one method: OCTA was the earliest detector in 40 eyes, or 37.4% Circumpapillary retinal nerve fiber layer OCT was earliest in 32 eyes, or 29.9% Visual-field testing was earliest in 26 eyes, or 24.3% These figures do not mean that OCTA was correct in 37.4% of all patients. They mean that among eyes in which at least one test detected progression, OCTA was the first test to cross that study’s threshold in about one-third of cases. Specificity and false-positive rates Among 45 eyes considered stable, reported specificity was: OCTA: 68.9% Circumpapillary retinal nerve fiber layer OCT: 75.6% That corresponds to approximate false-positive rates of: OCTA: 31.1%, or about 14 of the 45 stable eyes Circumpapillary retinal nerve fiber layer OCT: 24.4%, or about 11 of the 45 stable eyes This is an important limitation. The OCTA signal appeared earlier, but it was also less specific than the structural OCT measurement. The study did not report a conventional sensitivity against an independent gold standard because there is no perfect gold standard for slow glaucoma progression. Visual fields cannot serve as a completely independent reference when the question is whether OCTA detects change before visual fields. The number 58 of 107 progressing eyes, or approximately 54%, is a detection proportion, not a true sensitivity. Exact lead time The reported mean lead times were: OCTA before visual-field progression: 2.3 years 95% confidence interval: 1.3 to 3.2 years Circumpapillary retinal nerve fiber layer OCT before visual-field progression: 1.5 years 95% confidence interval: 0.6 to 2.4 years OCTA versus structural OCT: 0.2 years 95% confidence interval: −0.6 to 0.9 years That last comparison is crucial. The study did not show a clear two-year advantage over structural OCT. The difference between OCTA and retinal nerve fiber layer OCT was only 0.2 years, and the confidence interval included no difference and even favored structural OCT slightly. Therefore: > The strongest finding was that OCTA crossed its progression threshold earlier than visual fields. The evidence that OCTA is meaningfully earlier than structural OCT is weak. Why the Two-Year Advantage Should Not Be Accepted at Face Value It is a comparison of thresholds, not necessarily disease onset Visual-field progression is difficult to detect because visual-field testing is noisy. A test may need several abnormal results before the Guided Progression Analysis labels progression. OCTA may therefore appear to lead visual fields for two reasons: OCTA detected genuine earlier biological change. The visual field required more time and more repeated tests to overcome measurement noise. The study cannot fully distinguish these possibilities. The definition of progression was not identical across tests OCTA and OCT were considered positive when a measurement exceeded test-retest variability on two consecutive visits. Visual fields used Guided Progression Analysis. These algorithms ask different questions: OCTA asks whether a quantitative imaging measurement fell beyond an expected repeatability boundary. Structural OCT asks whether tissue thickness changed beyond its own boundary. Visual-field analysis asks whether sensitivity at selected points worsened beyond expected variability. A test with a lower threshold or greater biological responsiveness will tend to be classified as “earlier,” even if it is not more accurate. The study was retrospective and based on a referral cohort The Diagnostic Innovations in Glaucoma Study is valuable, but it is not a random sample of the general glaucoma population. Referral-center cohorts often contain: More atypical cases More established glaucoma More patients with suspicious or borderline findings More frequent imaging than ordinary clinical practice The results may not apply equally to patients with mild glaucoma, ocular hypertension, high myopia, cataract, diabetes, or poor-quality scans. The stable group was small The specificity estimate was based on only 45 stable eyes. A small change in the number of apparent false positives could substantially change the reported specificity. “Earlier” did not necessarily mean “actionable” An OCTA measurement might decline two years before the field crosses a statistical threshold, but the clinician still needs to know: Is the decline repeatable? Is it topographically consistent with the retinal nerve fiber layer or ganglion-cell layer? Is it still present after signal-strength correction? Could it reflect blood pressure, intraocular pressure, medication, or cataract changes? Does it predict future visual disability? The study did not establish that an OCTA alert should automatically lead to treatment escalation. Could the Early OCTA Signal Be an Artifact? Yes. Several explanations are biologically plausible. Visual-field noise Standard automated perimetry varies because of: Attention Fatigue Learning effects False-positive responses False-negative responses Fixation instability Dry eye and blinking Anxiety Advanced damage at the tested location The variability is often greater at already damaged locations. Guided Progression Analysis is designed to reduce false alarms, but false positives still occur. In one analysis of stable visual fields, the five-year cumulative false-positive rate was approximately 34% for “possible progression” and 7% for “likely progression.” Global mean-deviation and visual-field-index trend criteria had lower five-year false-positive rates of approximately 4% to 5%. Visual-field progression anal Support the show

This audio article is from VisualFieldTest.com. Read the full article here: https://visualfieldtest.com/en/scientists-found-a-new-abnormality-inside-human-glaucoma-nerve-cells-could-it-lead-to-a-new-treatment Test your visual field online: https://visualfieldtest.com Support the show so new episodes keep coming: https://www.buzzsprout.com/2563091/support Excerpt: Scientists Found a New Abnormality Inside Human Glaucoma Nerve Cells — Could It Lead to a New Treatment? Short answer: Possibly—but the evidence is still early. A newly published human donor-retina study found that glaucoma was associated with less sphingomyelin inside retinal ganglion cells, more acid sphingomyelinase protein, and greater activity of the lysosomal form of that enzyme. The study also found more retinal ganglion cells containing ceramide aggregates, although total ceramide was not significantly higher overall. That pattern is biologically interesting because acid sphingomyelinase can break down sphingomyelin into ceramide. Excessive or mislocalized ceramide can disturb lysosomes, cell membranes, autophagy, mitochondria, inflammatory signaling, and programmed cell death. However, the human study is observational and postmortem. It does not prove that acid sphingomyelinase starts glaucoma or that inhibiting it will preserve vision. The strongest evidence for causality still comes from animal and cell studies, not from patients. > My overall interpretation: Acid sphingomyelinase is a credible contributor to retinal ganglion-cell injury in at least a subset of glaucoma, but it is unlikely to be the only cause or a universal treatment target. --- What the New Human Study Actually Found The newest study, published online on August 31, 2026, examined donated human retinas from people with and without a glaucoma diagnosis. It used a sphingomyelin-binding probe called enhanced green fluorescent protein-conjugated non-toxic lysenin and identified retinal ganglion cells using the retinal ganglion-cell marker RNA-binding protein with multiple splicing. The researchers also measured acid sphingomyelinase, neutral sphingomyelinase, sphingomyelin synthase 1, sphingomyelin synthase 2, enzyme activity, and ceramide distribution. Human glaucoma donor-retina study () What can be determined from the currently accessible report? For the full table, please open this article on visualfieldtest.com. The article is currently labeled an early accepted version that may undergo further editing before the final version of record. Therefore, exact numeric values should be taken from the full downloadable article and supplementary data once they are accessible in a stable form, rather than reconstructed from figures or secondary summaries. Scientific Reports article page () The most important negative finding The study did not show a simple, uniform increase in total ceramide throughout the retina. That matters. A straightforward model would predict: > More acid sphingomyelinase → less sphingomyelin → more total ceramide. Instead, the study found: > Less sphingomyelin in retinal ganglion cells → more acid sphingomyelinase → more ceramide-containing aggregates, but no statistically significant increase in total retinal ganglion-cell ceramide. This suggests that the important abnormality may be local ceramide clustering, rather than a large increase in the average ceramide concentration across the whole retina. That is biologically plausible because ceramide can act as a membrane-organizing signal. A small amount concentrated in the wrong lysosomal or plasma-membrane domain may be more damaging than a larger amount dispersed throughout the cell. --- Why the Study Is Interesting but Not Yet Proof of Cause The human findings support a coherent mechanism, but several alternative explanations remain possible. Acid sphingomyelinase may increase because retinal ganglion cells are already dying Damaged neurons often activate lysosomal enzymes, inflammatory pathways, and membrane-recycling systems. Therefore, increased acid sphingomyelinase could be: an early cause of retinal ganglion-cell injury; a response to mechanical, vascular, or metabolic injury; or a late consequence of degeneration. The human study cannot determine the timing because postmortem tissue provides only one snapshot. Lower sphingomyelin may partly reflect cell loss Glaucomatous retinas contain fewer retinal ganglion cells. A whole-retina dot blot can therefore show lower sphingomyelin simply because the tissue contains fewer sphingomyelin-rich neurons. The cell-level analysis is stronger because it compares sphingomyelin labeling in identified retinal ganglion cells. Even then, survivor bias remains possible: the analysis may compare surviving glaucoma retinal ganglion cells with healthy cells while missing the most severely damaged cells that have already disappeared. The lysenin probe does not measure every sphingomyelin species equally Enhanced green fluorescent protein-conjugated lysenin preferentially binds certain, especially longer-chain, sphingomyelin species. It is therefore best interpreted as a measure of accessible membrane-associated sphingomyelin, not necessarily a complete measurement of every sphingomyelin molecule in the cell. Visualizing sphingomyelin in the retina () Postmortem tissue is vulnerable to artificial biochemical changes Important limitations include: postmortem delay, which can alter lysosomal pH and enzyme activity; hypoxia or agonal illness before death; systemic infection, diabetes, vascular disease, or inflammation; cause of death; age and sex differences; glaucoma medications; antidepressant or antihistamine exposure; retinal region sampled; fixation and tissue-processing differences; incomplete removal of vitreous or other surrounding tissue; loss of fragile or already-degenerated cells; uncertainty about the exact glaucoma subtype and severity. These factors are particularly important because acid sphingomyelinase is a stress-responsive enzyme. --- Reconstructing the Proposed Pathway The proposed pathway is: > Acid sphingomyelinase activation → sphingomyelin breakdown → ceramide generation and clustering → lysosomal and membrane dysfunction → mitochondrial stress → apoptosis → retinal ganglion-cell and axon loss Each step has a different level of evidence. Step 1: Acid sphingomyelinase activation Acid sphingomyelinase is encoded by the SMPD1 gene. Its main form is located inside lysosomes, where it works best in an acidic environment. A separate form can be processed and secreted outside the cell. The lysosomal form is often described as the zinc-independent pool, whereas secreted acid sphingomyelinase is more dependent on zinc at neutral extracellular pH. The new human study found increased retinal ganglion-cell acid sphingomyelinase expression and increased zinc-independent activity, while the secretory pool did not significantly change. That pattern points toward an intracellular lysosomal abnormality rather than a generalized rise in circulating or extracellular enzyme. Step 2: Sphingomyelin breakdown Acid sphingomyelinase converts sphingomyelin into: ceramide; phosphorylcholine. Sphingomyelin is not merely structural fat. It contributes to: plasma-membrane stability; membrane thickness and order; lipid-raft organization; receptor signaling; lysosomal membrane properties; vesicle trafficking. The 2022 retinal and optic-nerve-head study found that sphingomyelin species were concentrated in the retinal ganglion-cell layer, optic nerve, and choroidal regions. In experimental ocular hypertension, retinal acid sphingomyelinase activity increased from approximately 54.98 mU/mg protein at baseline to 121.6 mU/mg protein, about a 2.2-fold increase. In the optic nerve head, activity increased from approximately 95.6 to 267.0 mU/mg protein, about a 2.8-fold increase. Sphingomyelinases in retinas and optic nerve heads () Step 3: Ceramide accumulation and clustering Ceramide is a signaling lipid, not simply a waste product. Depending on its chain length, location, and concentration, ceramide can: promote membrane-domain formation; cluster death receptors; alter calcium handling; impair vesicle trafficking; affect lysosomal stability; stimulate inflammatory signaling; disrupt mitochondrial membranes; activate caspases and apoptosis. The new human glaucoma study suggests that ceramide aggregation in selected retinal ganglion cells may be more important than total retinal ceramide. This would explain why whole-tissue lipidomics may fail to detect a large increase: the damaging signal may be concentrated in a small number of vulnerable cells. Step 4: Lysosomal and autophagy dysfunction Lysosomes must maintain a precise lipid composition. Too much sphingomyelin can impair lysosomal function, but too little acid sphingomyelinase can also be harmful. This is demonstrated by acid sphingomyelinase-deficient mice. Complete deletion caused: progressive photoreceptor degeneration; reduced electroretinogram responses; retinal pigment epithelium dysfunction; lipofuscin accumulation; abnormal sphingomyelin and sphingosine accumulation; increased autophagosome-associated protein. Lack of acid sphingomyelinase induces age-related retinal degeneration () This is a critical warning: complete acid sphingomyelinase blockade is not a safe therapeutic goal. The likely goal would be partial, localized, and disease-stage-specific reduction. Step 5: Mitochondrial stress Retinal ganglion cells are highly energy-dependent neurons with long axons. Mitochondrial dysfunction is an established early Support the show