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New research reveals how low blood sugar can damage the retina in diabetes, highlighting potential treatments targeting specific proteins to prevent vision loss.

Hypoglycemia may promote a breakdown of the blood-retinal barrier, study finds

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Susana Marcos, PhD, discusses the implications her research presents for the role optical coherence tomography (OCT) could play in presbyopia and myopia accommodation efforts.

ARVO 2025: Lens thickness as a significant biomarker for accommodation in presbyopia

The novel intraocular lens works to restore dynamic range of vision following cataract surgery.

US FDA gives Atia Vision go-ahead to begin clinical study of the OmniVu Lens System

The OTC eye drops contain low-dose brimonidine tartrate 0.025%.

Bausch + Lomb launches LUMIFY Preservative Free redness reliever eye drops in US

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Controversies in pediatric refractive development

A recent study has further underscored the potential of retinal imaging as a noninvasive and accessible screening tool for Alzheimer disease in a multimodal model that utilizes retinal and blood-based biomarkers that have been used to detect the disease.

 The study, led by first author Swetha Ravichandran, PhD student at the University of Alabama at Birmingham, found that combining retinal and blood-based biomarkers significantly improved diagnostic accuracy, particularly when using threonine-217 (p-tau 217) and plasma amyloidogenic beta residue 42/40 ratio (Aβ42/Aβ40 ratio).

“This could revolutionize early AD detection, facilitating earlier intervention, and improved disease management,” the study authors stated.

The study authors also noted that while previous studies have shown that blood-based and retinal biomarkers have shown potential to identify patients that may be at risk for Alzheimer disease, integrating the 2 types of biomarkers has not been adequately assessed in preclinical Alzheimer disease.

 “This concept introduces a novel and synergistic approach to improve screening accuracy and predictive capability for early AD detection,” the researchers stated.

By using a multimodal receiver operating characteristic model based on retinal biomarkers (gliosis area, inner inferior retinal nerve fiber layer [RNFL] thickness) and plasma biomarkers (p-tau217 and Aβ42/Aβ40 ratio), researchers observed an area under the curve (AUC) of 0.97 (95% CI = 0.93–1.01) when compared to unimodal models of retinal and plasma biomarkers. Researchers also evaluated the diagnostic value of neurofilament light (NfL) and threonine-181 (p-tau181).

“A single retinal biomarker may not be sensitive or specific to AD. This is because these retinal biomarkers are also affected by other retinal diseases. Even though we clinically excluded comorbid retinal conditions, it is difficult to distinguish preclinical manifestations of these comorbid retinal conditions from retinal changes that occur in preclinical AD,” the study authors stated. “For example, putative retinal gliosis is indicated in other retinal conditions that have neuroinflammatory components such as glaucoma, diabetic retinopathy, and [epiretinal membrane]. While the above retinal diseases were clinically excluded from our study, it is possible that some of the retinal changes observed could be preclinical manifestations of these conditions.”

A total of 82 cognitively unimpaired participants, and 141 eyes, who were previously involved in the Atlas of Retinal Imaging in Alzheimer’s Study (ARIAS), were included in the study. Inclusion criteria for the study included the absence of or controlled hypertension (blood pressure < 140/90), hyperlipidemia (total cholesterol ≤ 240 mg/dL), and systemic diabetes (HbA1c ≤ 7). All eyes in the study had a best corrected visual acuity of ≥ 20/40 (~ Log MAR 0.30) and refractive errors ≤ ± 3.00 DS (spherical equivalent) or equivalent axial lengths (range: 22–24 mm) in order to prevent any significant differences in the retinal magnification, per the Bennett formula.

Participants also underwent comprehensive neuropsychological assessment using the MoCA and the RBANS-U. Spectral domain optical coherence tomography images were obtained, and plasma sampling and analysis were conducted for the study. With 32 participants having received recent Aβ PET neuroimaging, the results were also made available to the ARIAS study team.

A significant correlation was also found between putative retinal gliosis and p-tau217 in the univariate mixed model (

 = .007) but not for the other plasma biomarkers evaluated (

 > .05). Additionally, a sensitivity of 93.8% and a specificity of 92% was observed in the Aβ42/Aβ40 ratio.

Study authors noted that future research should work to validate the findings of the study in larger, more diverse populations, in addition to evaluating the longitudinal impact of retinal changes in Alzheimer disease progression. Biological mechanisms linking the disease pathology to putative retinal gliosis could also provide an opportunity to understand more about said pathology and therapeutic targets.

Ravichandran S, Snyder PJ, Alber J. Association and multimodal model of retinal and blood-based biomarkers for detection of preclinical Alzheimer’s disease. 

2025;17:19. https://doi.org/10.1186/s13195-024-01668-5

The recent study details the diagnostic value of a multimodal model utilizing both types of biomarkers when compared with unimodal models.

Researchers find Alzheimer disease detection potential in blood-based, retinal biomarkers

At this year’s ASCRS meeting, the Eye Care Network sat down with Karl Stonecipher, MD, to discuss some of the most exciting clinical outcomes and technological advancements in refractive surgery—particularly in the treatment of high myopia. Stonecipher shared insights from a recent trial using the Teneo laser platform (Bausch + Lomb), highlighting its speed, precision, and patient-centered design. He delves into real-world outcomes, including a remarkable 98% to 99% satisfaction rate among patients, minimal dysphotopsias, and stable postoperative vision, even in high myopes.

Q&A with Karl Stonecipher, MD, about LASIK results in patients with high myopia

Q: What were the key figures that we were kind of excited about with regard to outcomes in this particular arm of the trial? 

So we're really looking at high myopia. So we're talking about -8. The average for the study was about -5, -5.6, but I want to go back and say what I'm excited about the laser first, and what the laser does to get the outcomes. It's a GUI interface, which is really easy to understand. My staff loves that. It's very comfortable for the patient, and it's extremely fast at 1.2 seconds per diopter. I think a lot of that has to do with the outcomes of over 98% of the patients doing extremely well and very satisfied with the outcomes, with amazing stability.

Q: What kind of dysphotopsias are we seeing post LASIK with this laser platform, and how do the patients report that and respond to it? 

Since we all know that when we first started with higher myopes, we're concerned about spherical aberration, and we're actually showing that we're getting improvement from baseline to present day. And so what happens is, patients come in, we don't see as much glare and halos. The PROWL questionnaire is obviously what we use, and we show improvements across all platforms at this high level, and we don't see dysphotopsias like we saw with a lot of those earlier platforms.

Q: Are patients satisfied with Teneo results?

Well, I can tell you that with patient satisfaction, we had some of the highest rates we've ever had: 98%, 99% saying that they would recommend it to families and friends. They would do it again if they had to. So obviously, at those levels, you can't please everybody. You can't make everybody happy. You know, you'd love to make all of them smile and walk out the door, but [I've] got to tell one anecdote. And I'm not sure if this is great, but one of the patients postop said to me, I love you almost as much as I love Jesus now. So obviously that's a good thing in terms of the outcome. So I think that we're happy that patients are happy. But we also now have these questionnaires. So they're happy in low light, they're happy in bright sunny days. They're happy in... they're getting up to go hunting or they're getting up to take their kids to school. So I think that's important.

Q: What do you like about the Teneo platform?

So the Teneo is a new platform. I like to tell you the things that I like about it. The No. 1 thing that I like about it any surgeon, especially my residents and fellows that work with me, are what...they're concerned about what do I put in the box? What do I put in the laser? So what's the manifest refraction? So we're talking about high myopia. We just put the manifest in the box. This is not nomogrammed information, and you had 20/20, 20/25 level of vision that was stable in the high 90 range. And so patients are coming back happy, and it's the surgeon's comfort. Now, don't get me wrong, I'm sure we're going to nomogram things down the road to even fine-tune that more, but this is off the manifest refraction. So we're not cycloplegia-ing these patients anymore. We're not having to do... with the nonmydriatic cameras we can look at the retina. So if I see something abnormal in the retina, then I'm going to send this patient category off to see the retinologist, because it's important at this level to make sure they don't have any holes or tears. But it's a very convenient laser, because you can come in, I can manifest you, you don't have to go through the dilation process, and get great outcomes.

Conference

Q&A with Karl Stonecipher, MD, on outcomes of LASIK using the Teneo platform to correct high myopia

New studies supported by the National Institutes of Health’s (NIH) National Eye Institute (NEI) Intramural Research Program suggest that the drug reserpine, approved for high blood pressure in 1955, has the potential of treating retinitis pigmentosa in the form of a small molecule therapy. Currently, no therapy exists for the inherited retinal disease (IRD).

 The studies were published in a singular report in 

“The discovery of reserpine’s effectiveness may greatly speed therapeutics for retinitis pigmentosa and many other inherited retinal dystrophies, which can be caused by one of more than a thousand possible mutations affecting more than 100 genes. Reserpine’s neuroprotective effect is independent of any specific underlying gene mutation,” said the study’s lead investigator, Anand Swaroop, PhD, senior investigator at NIH’s National Eye Institute, in the release.

In the latest study, researchers evaluated the therapeutic potential of reserpine for autosomal dominant retinitis pigmentosa, a dominant form of the disease caused by a mutation in the visual pigment gene rhodopsin, by using a P23H-1 rat model and performing a series of assays to evaluate the response to reserpine treatment on retinal pathology. Reserpine was administered via intraperitoneal injection, with data collected through optokinetic tracking; ERG recordings; fundus imaging and optical coherence tomography; immunohistochemistry; RNA extraction and library preparation; and RNA-seq and data analysis.

Evidence from the studies showed that reserpine improves survival of photoreceptor cells, the light-detecting retinal neurons that die due to retinitis pigmentosa and other retinal dystrophies. Compared to untreated rates, reserpine preserved the process in which photoreceptors convert light that enters the eye into electrical signals that are sent to the brain to produce vision, known as phototransduction, in rod photoreceptors.

 “The neuroprotective effect of reserpine was achieved, at least in part, through the restoration of the balance between autophagy and the ubiquitin-proteasome system, the stress-response pathways maintaining cellular proteostasis,” the study authors stated.

Additionally, reserpine produced better protective effects for rod photoreceptors in female rats in comparison to male rats. Researchers also noted that significant preservation of cone photoreceptors was found more often in female rats compared to male rats.

“We can only speculate about these sex-specific differences. However, future research would benefit from teasing out these differences and understanding them to lay a foundation for personalized approaches to retinal disease therapy,” Swaroop said in the release.

Swaroop and his research team are also developing additional and more potent reserpine-related drugs to be used as options to treat late-onset or slowly progressing IRDs. These drugs may also be able to stall vision loss in different types of aggressive retinitis pigmentosa until more effective treatments are developed that can reverse said vision loss.

Although reserpine is no longer being used for treating high blood pressure due to its adverse effects, researchers hope that the low required dosage for treating retinal degeneration would quell said effects, according to the release.

Researchers note that the molecular target of reserpine in the retina remains unknown, while acknowledging the possibility for a different association in the retina. The reasons for biological sex bias in drug response must also be investigated, particularly whether retinas in female and male rats are predisposed differently to retinal pathology and interventions. “Overall, our findings highlight the broader application of small molecules derived from unbiased large-scale screening and underscore the importance of considering sex-specific differences in the development of treatments for IRDs,” the study authors stated.

Repurposing a blood pressure drug may prevent vision loss in inherited blinding diseases. News release. National Institutes of Health. April 15, 2025. Accessed May 6, 2025. 

https://www.nih.gov/news-events/news-releases/repurposing-blood-pressure-drug-may-prevent-vision-loss-inherited-blinding-diseases

Song HB, Campello L, Mondal AK, et al. Sex-specific attenuation of photoreceptor degeneration by reserpine in a rhodopsin P23H rat model of autosomal dominant retinitis pigmentosa. 

The drug was previously approved for high blood pressure in 1955.

Reserpine has potential to be repurposed as treatment for retinitis pigmentosa, studies suggest

Neda Shamie, MD; Selina McGee, OD, FAAO, Dipl ABO; and Jacob Lang, OD, FAAO; provided their insights during CIME 2025 on May 4.

CIME 2025: What you missed in presbyopia tips, tricks, and updates

A plethora of topics were discussed from a collaborative care perspective at this year's annual Controversies in Modern Eye Care (CIME) conference in Los Angeles, California. From lenses to eye drops, presbyopia was a particularly hot topic on May 4. Neda Shamie, MD; Selina McGee, OD, FAAO, Dipl ABO; and Jacob Lang, OD, FAAO, detail key takeaways on presbyopia from CIME 2025.

Pharmacological presbyopia treatment is definitely something that we've been thinking about for a long time. It is a kind of a holy grail of eye care. Everyone over the age of 45 develops presbyopia, so to have a solution to bridge those patients until they develop cataracts or significant symptomatic changes of their vision, it's really important to think about solutions for our patients and eye drops. Presbyopia drops are a fantastic option for the right patient. It's ideal for that niche patient, the one who's between 45 and about 55 who is starting to have presbyopia. 

An ideal patient would be an emmetrope who's really enjoyed excellent vision for a long time and is starting to have difficulty with their near vision. There's really no surgical grade option for them. Definitely, spectacles are great. Contact lenses with mono vision are great, but then drops offer an additive, or kind of a complementary option for these patients. What's exciting are all the improvements in the presbyopia drop kind of options that we have available. Thus far, we have had the 1.25% pilocarpine, which has been great and some patients really respond nicely to it. But because of the higher concentration of the pilocarpine, there are [adverse] effects associated with it. 

So now recently, there was a new eye drop the pilocarpine 0.4% that has been FDA approved and available to us. Really exciting, lower concentration of pilocarpine, less [adverse] effect profile and yet equal response. The vehicle of this drop is soothing to the ocular surface. And really it's 2-in-1 in a sense. And many of these patients really have ocular surface disease that contributes to their visual problems. And so the new 0.4% pilocarpine offers ocular surface soothing effect with a vehicle together with a lower dose of pilocarpine.

Presbyopia is one of those really frustrating conditions for patients, and they don't understand all their options. They don't even understand that they can have multiple options. And I think that's the biggest key, is we want to prescribe for specific situations, and that might be a pair of spectacles and a therapeutic drop, it might be contact lenses and spectacles and a therapeutic drop, it might be a surgical option and a therapeutic drop. So I think we have to get out of this mindset. And our patients certainly don't understand this, that there's more than one option, and they're allowed to have more than one option, and so I think it's just really important that we give patients all of the available therapies and all the available technologies we have great candidates for therapeutic interventions with presbyopia are patients that are motivated.

Ultimately, it's not finding the right exact prescription or the right exact pupil size. It's more about is the patient motivated to try something different and be less dependent on their current technology. When you are examining your patient and you're talking about pharmaceutical options for presbyopia, you're going to do everything that you already do. It's going to make sure that the patient is a good candidate for the prescription therapy, and that means looking at their retina, whether it's a wild field photo or it's a dilated eye exam, as long as you can look and make sure they don't have any retinal pathology or anything else that would preclude them from being able to use it. It's the things that you and I already do. So just make sure that patient's had a comprehensive eye exam and then move forward with your therapies from there.

What excites me most about pharmacological correction for presbyopia is really a new option. The flexibility that pharmacological options give our patients to use it when they need it, and be able to give them some freedom, flexibility and lifestyle options for their busy lives and busy careers through these busy presbyopic years is really what excites me most. 

Some of the barriers that patients run into with regard to pharmacologic correction and presbyopia, I think one of the biggest ones is their providers. [It] is actually the doctors not knowing what options are out there with regards to pharmacologic correction and how those pharmacologic options might benefit their patients in their chairs. So furthering their education, embracing new things. I think that's the biggest thing and the biggest barrier to patients getting access to these options. When we're thinking about our patients and taking care of our patients, if we're prescribing any sort of treatment option, we want to do the best for our patients first, right? Do no harm. So we've got to take care of our patients from tea to green, from ocular surface to retina, optic nerve, we've got to take care of the entire patient. And that's why it's so important that we're the doctor, that this is really, you know, we're talking about presbyopia correction with pharmaceuticals. This is an eye drop in an eye drug. And so eye doctors need to take the role there and be the doctor. Take care of the entirety of the globe, the entirety of their ocular health from front to back.

Neda Shamie, MD; Selina McGee, OD, FAAO, Dipl ABO; and Jacob Lang, OD, FAAO, provided their insights during CIME 2025 on May 4.

. I’m big on semantics and will debate them with you ad nauseam. Our clinical lifetimes are lifetimes of practicing what we do, and it takes practice. With that notion in mind, this issue’s column will be comprised of several facts about glaucoma that I have picked up along the way.

Your patients are not taking their medications like they say they are. Neither are mine. Adherence issues are at or near the top of avoidable barriers to proper glaucoma treatment. I will not bore you by rattling off study after study, but a simple search of the world’s peer-reviewed literature will yield substantial evidence supporting the fact that adherence remains an issue. For this reason, I have gotten away from adding a third drop to a patient’s regimen. Adherence tends to go down significantly when that third drop is added. I typically consider a prostaglandin analogue or facsimile thereof at night and a combination drop twice a day for maximum medical therapy. If the target IOP is not achieved, we are heading toward a consultation for selective laser trabeculoplasty (SLT) and/or minimally invasive glaucoma surgery. More on this later.

Visual field studies stink. They always have, and they always will. However, I do not foresee a time in my clinical lifetime when we are not performing them. Patients are either trigger-happy or asleep at the wheel. Furthermore, there is no holy grail visual field analyzer for all stages of glaucoma. Yes, frequency-doubling technology does seem to pick up glaucomatous defects earlier at times. However, there is no visual field analyzer that is optimal for all stages of glaucoma. With that said, as much as visual field studies stink, they need to be repeated. If you take nothing else from this column, remember to repeat the visual fields study. Reliable and repeatable defects are part of what drives treatment in one direction or another.

A decent number of patients with glaucoma—even younger ones—will present with normal IOPs. In fact, the contemporary definition of glaucoma does not mention IOP. It’s just a risk factor (thankfully, a modifiable one because it is the No. 1 risk factor). When a teenager comes in with suspicious optic nerve heads and IOPs of 11 mm Hg, a workup is still necessary. You are getting a snapshot of that patient’s IOP throughout the course of a day. I am not saying you need to spend the day with that patient, but I am saying you should consider bringing the patient back at a different point in the day over several visits to perhaps detect an overall trend. One IOP reading does not make or break a glaucoma diagnosis, regardless of patient age.

There will be patients with glaucoma whom you do not treat. I can promise you that. I have one patient who had to take a lot of prednisone over the course of her life. When she had a curative surgical procedure, she no longer needed steroids. Another optometrist referred her to me as suspicious for glaucoma, and I am convinced that she was a steroid responder and acquired moderate glaucomatous damage from it. Her IOPs are low, and results from serial visual field studies, optical coherence tomography studies, and optic nerve evaluations have shown no progression. I eventually went from seeing her every 3 months to every 6 months and have been doing so for 12 years now.

Patient history is as important as they taught you it was in optometry school—maybe even more so. Some favorite questions of mine that I always ask during an examination are the following: Do you get headaches around your eyes (IOP spiking)? Do you ever see halos around lights (transient angle closure)? Did you ever get really sick in the past and require hospitalization or coma (history of hemodynamic crisis)? Did you ever have to take steroids for an extended period (this damage may be old news)? Do any of your blood relatives have glaucoma? That last one requires a follow-up question if the answer is yes. I want to know about a family history of glaucoma, but I also want to know how that family member is doing. A grandfather who takes a prostaglandin analogue, lives independently, and has great vision represents a much different scenario from a sister who has to hold onto walls to get around. That follow-up question will likely play a role in your treatment of the patient.

Finally, put yourself in your patient’s shoes. Since I have started to make a concerted effort to do this, it has changed my perception of myself—specifically my delivery of information. I have also asked myself what I would do if I found out that I had glaucoma, and the very likely scenario is that I would be in line for SLT. I would want to avoid medical therapy if at all possible. This (thankfully) hypothetical question has garnered more support over the past few years, as we now have good evidence that SLT is safe, effective, and cost-effective when compared with medical therapy (insert plug for state political action committee contribution here).

This list is intended to be progressive in nature. Help me add to it! What tangible information have you picked up along the way? Let’s compare and contrast with the goal of advancing the collective consciousness surrounding glaucoma.

Knowing the truths concerning patient adherence and history and visual field tests can make a difference in care quality.

What to keep in mind when diagnosing and treating glaucoma

At ARVO 2025, Mark Bullimore, MCOptom, PhD, emphasized the need for more accurate, condition-specific tools in evaluating myopic eye growth and treatment efficacy.

ARVO 2025: Rethinking centile growth curves in myopia management with Mark Bullimore, MCOptom, PhD

At the 2025 ARVO conference in Salt Lake City, Mark Bullimore, MCOptom, PhD, of the University of Houston College of Optometry shared a compelling critique of the current use of centile growth curves for axial length in myopia management. Speaking directly to optometrists, Bullimore emphasized the need for more accurate, condition-specific tools in evaluating myopic eye growth and treatment efficacy.

The problem with conventional growth curves

Centile growth curves—long used in pediatrics to track height and weight—are increasingly being applied to axial length measurements in children. According to Bullimore, this is where the utility of these curves begins and ends in the context of myopia.

"These curves are based on data from all children, not just myopic ones," he explained. "So they substantially underestimate axial elongation in myopic children."

This limitation has 2 major consequences:

 The curves fail to reflect how fast a myopic child's eye is likely to elongate.

 They hinder clinicians from accurately determining whether myopia control treatments are working.

Bullimore also cautioned against relying on axial length alone to predict myopia onset. While it has some predictive value, "cycloplegic refractive error is far more accurate," he said.

To manage myopia effectively, Bullimore recommends using data derived solely from myopic children. This would allow practitioners to assess the expected axial elongation in untreated cases and compare it meaningfully against treated ones.

“What you want is to know how quickly the average untreated myopic child’s eye will grow,” he said. “And ideally, you’d have confidence intervals or centile ranges 

By separating myopic from nonmyopic data, clinicians can gain a more realistic benchmark and better evaluate the success of interventions like orthokeratology or low-dose atropine.

Bullimore’s insights at ARVO underscore the importance of precision in pediatric myopia care. As the prevalence of childhood myopia continues to rise, refining the tools we use to monitor progression and assess treatment outcomes is more critical than ever.

Timothy E. Hug, OD, FAAO

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