Category: Ophthalmology

Categories : Implants and Prostheses OphthalmologyTags :

Common Eye Ointment can Damage Glaucoma Implants, Study Warns

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Research shows that petrolatum-based eye ointments can cause the device to swell and potentially rupture, prompting an urgent update to clinical guidance.

Photo by Tima Miroshnichenko


Widely-used eye ointments can cause glaucoma implants to swell and potentially rupture, according to new research from Nagoya University in Japan. This study is the first to show, using clinical and experimental evidence, that petrolatum-based eye ointments can compromise the PRESERFLO® MicroShunt, an implant used in over 60 countries to treat glaucoma.

Glaucoma is an eye disease that damages the optic nerve and can lead to vision loss. It often results from increased intraocular pressure caused by blocked drainage of eye fluid. A recent study estimated that 76 million people globally are affected by glaucoma.

Progression of visual field loss (from left to right) due to glaucoma
(Credit: Ryo Tomita)

MicroShunt is a small filtration device implanted in the eye to improve fluid drainage in glaucoma patients. Compared to traditional surgeries, it lowers post-operative complications and reduces reliance on additional medications.

MicroShunt is made from a styrenic thermoplastic elastomer based on a polystyrene-block-polyisobutylene-block-polystyrene (SIBS) block polymer, which is highly biocompatible, flexible, and less likely to cause inflammation or scarring. However, this material is vulnerable when it comes into contact with hydrocarbon- and oil-based materials. Due to its high oil affinity, exposure to petrolatum-based eye ointments may allow oil components to penetrate the device, causing swelling and potential changes in its shape and flexibility.

The MicroShunt manufacturer’s instructions state that “the MicroShunt should not be subjected to direct contact with petrolatum-based (ie, petrolatum jelly) materials, such as ointments and dispersions.” But this precaution is not widely recognised or consistently followed in clinical practice.

“Swollen MicroShunts can be structurally fragile,” said ophthalmologist and Assistant Professor Ryo Tomita of Nagoya University Graduate School of Medicine, the study’s first author. “During surgery, I observed a rupture in a swollen MicroShunt. If more clinicians are aware of this risk, they will be able to prevent similar problems.”

Tomita and colleagues, including Assistant Professor Taiga Inooka and Associate Professor Kenya Yuki from Nagoya University Hospital and the Graduate School of Medicine collaborated with Dr. Takato Kajita and Junior Associate Professor Atsushi Noro from the Graduate School of Engineering to examine changes in the MicroShunt after exposure to a petrolatum-based eye ointment.

The medical team reviewed clinical cases, while the engineering team conducted laboratory analyses. The findings were published in Graefe’s Archive for Clinical and Experimental Ophthalmology.

Clinical evidence

The clinical study examined seven glaucoma patients whose MicroShunt implants were later removed for different reasons. The results revealed a clear pattern. In three cases, the MicroShunt was exposed outside the conjunctiva, and patients received a petrolatum-based eye ointment. All three explanted devices showed significant swelling, and two of them ruptured.

In three other cases, the MicroShunt remained covered by the conjunctiva, and no ointment was administered. These devices retained their original structure. Crucially, in one additional case, the MicroShunt was exposed outside the conjunctiva, but no ointment was applied. The device did not swell. This indicates that direct contact with the ointment, rather than conjunctival rupture alone, is the primary cause of swelling.

Photographic comparison of MicroShunt illustrating size changes
Top: MicroShunt explanted from a patient, exhibiting diffuse swelling with fracture and loss of one fin
Middle: MicroShunt explanted from another patient, showing localized swelling around the fin
Bottom: Unused MicroShunt (control)
Scale: 1 division = 1 mm   
(Credit: Ryo Tomita)

Laboratory confirmation

Laboratory experiments confirmed the clinical findings. The team immersed unused MicroShunts in petrolatum-based eye ointment to reproduce the swelling seen in clinical cases. Microscopic measurements showed significant changes. After 24 hours in the ointment, the MicroShunt’s outer diameter increased to 1.44 times its original size, and the fin-like portion widened to 1.29 times its initial value.

Chemical analysis identified the cause of this change. After 24 hours of immersion, oil components made up approximately 45% of the MicroShunt’s total weight, rising to 73% after three months. These results confirmed the primary cause of swelling to be the absorption of oil-based ointment constituents into the material.

Clinical implications

The research team emphasises that clinicians should avoid using petrolatum-based ointments on patients with MicroShunt implants, particularly when the device is exposed outside the conjunctiva. Alternative post-operative treatments should be considered, while further research is needed to assess whether swelling impacts MicroShunt performance even when rupture does not occur.

“Our study found that commonly used medical materials can cause unexpected complications if their chemical properties and usage environments are not fully understood,” Noro stated. “From both medical and engineering perspectives, we emphasise the importance of understanding the chemical properties of medical materials and appropriately managing their usage environments.”

Paper information:

Ryo Tomita, Taiga Inooka, Takato Kajita, Hideyuki Shimizu, Ayana Suzumura, Jun Takeuchi, Tsuyoshi Matsuno, Hidekazu Inami, Koji M. Nishiguchi, Atsushi Noro, and Kenya Yuki. (2026) Petrolatum-based ointment application induces swelling of the PRESERFLO MicroShunt. Graefe’s Archive for Clinical and Experimental Ophthalmology
DOI: 10.1007/s00417-025-07075-2

Categories : Ophthalmology PaediatricsTags :

Babies Learning to See After Being Born Blind

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Photo by Jeffrey Riley on Unsplash

A study conducted by University of Louvain (UCLouvain), published in Nature Communications, shows that part of the brain of babies born blind is permanently altered, while another part remains surprisingly intact. Babies’ brains are much more adaptable than previously thought: even if they cannot see at the very beginning of life, they can later learn to recognise the world around them.

Some babies are born with early blindness due to dense bilateral congenital cataracts, requiring surgery to restore their sight. This period of several months without vision can leave a lasting mark on how the brain processes visual details, but surprisingly little on the recognition of faces, objects, or words.

Using brain imaging, the researchers compared adults who had undergone surgery for congenital cataracts as babies with people born with normal vision. The results are striking: in people born with cataracts, the area of the brain that analyses small visual details (contours, contrasts, etc.) retains a lasting alteration from this early blindness. On the other hand, the more advanced regions of the visual brain, responsible for recognising faces, objects, and words, function almost normally. These “biological” results have been validated by computer models involving artificial neural networks. This distinction between altered and preserved areas of the brain paves the way for new treatments. In the future, clinicians may be able to offer visual therapies that are better tailored to each patient.

“Babies’ brains are much more adaptable than we thought,” explains Olivier Collignon, Professor at University of Louvain (UCLouvain). “Even if vision is lacking at the very beginning of life, the brain can adapt and learn to recognise the world around it even on the basis of degraded information.”

These findings also challenge the idea of a single “critical period” for visual development. Some areas of the brain are more vulnerable to early vision loss, while others retain a surprising capacity for recovery. “The brain is both fragile and resilient,” adds Olivier Collignon. “Early experiences matter, but they don’t determine everything.”

Source: Université catholique de Louvain

Categories : Implants and Prostheses OphthalmologyTags :

Pioneering Retinal Implant Restores Reading Vision to Blind Eyes

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Study participant Sheila Irvine training with the device. Credit: Moorfields Eye Hospital

After being treated with an electronic eye implant paired with augmented-reality glasses, people with sight loss have recovered reading vision, reports a trial involving a UCL and Moorfields clinical researcher.

The results of the European clinical trial, published in The New England Journal of Medicine, showed 84% of participants were able to read letters, numbers and words using prosthetic vision through an eye that had previously lost its sight due to the untreatable progressive eye condition, geographic atrophy with dry age-related macular degeneration (AMD).

Those treated with the device could also read, on average, five lines of a vision chart; some participants could not even see the chart before their surgery.

The trial, with 38 patients in 17 hospital sites across five countries, was testing a pioneering device called PRIMA, with Moorfields Eye Hospital being the sole UK site. All patients had lost complete sight in their eye before receiving the implant.

Dry AMD is a slow deterioration of the cells of the macula over many years, as the light-sensitive retinal cells die off. For most people with dry AMD, they can experience a slight loss of central vision. Through a process known as geographic atrophy (GA), it can progress to full sight loss in the eye, as the cells die and the central macula melts away. There is currently no treatment for GA, which affects 5 million people globally. All participants in this trial had lost the central sight of the eye being tested, leaving only limited peripheral vision.

This revolutionary new implant is the first ever device to enable people to read letters, numbers and words through an eye that had lost its sight.

Mr Mahi Muqit, associate professor in the UCL Institute of Ophthalmology and senior vitreoretinal consultant at Moorfields Eye Hospital, who led the UK arm of the trial, said: “In the history of artificial vision, this represents a new era. Blind patients are actually able to have meaningful central vision restoration, which has never been done before.

“Getting back the ability to read is a major improvement in their quality of life, lifts their mood and helps to restore their confidence and independence. The PRIMA chip operation can safely be performed by any trained vitreoretinal surgeon in under two hours – that is key for allowing all blind patients to have access to this new medical therapy for GA in dry AMD.”

The procedure involves a vitrectomy, where the eye’s vitreous jelly is removed from between the lens and the retina, and the surgeon inserts the ultra-thin microchip, which is shaped like a SIM card and just 2mm x 2mm. This is inserted under the centre of a patient’s retina, by creating a trapdoor into which the chip is posted. The patient uses augmented-reality glasses, containing a video camera that is connected to a small computer, with a zoom feature, attached to their waistband.

Around a month or so after the operation, once the eye has settled, the new chip is activated. The video camera in the glasses projects the visual scene as an infra-red beam directly across the chip to activate the device. Artificial intelligence (AI) algorithms through the pocket computer process this information, which is then converted into an electrical signal. This signal passes through the retinal and optical nerve cells into the brain, where it is interpreted as vision. The patient uses their glasses to focus and scan across the main object in the projected image from the video camera, using the zoom feature to enlarge the text. Each patient goes through an intensive rehabilitation programme over several months to learn to interpret these signals and start reading again.

No significant decline in existing peripheral vison was observed in trial participants.

These findings pave the way for seeking approval to market this new device.

Sheila Irvine, one of Moorfields’ patients on the trial who was diagnosed with age-related macular degeneration, said: “I wanted to take part in research to help future generations, and my optician suggested I get in touch with Moorfields. Before receiving the implant, it was like having two black discs in my eyes, with the outside distorted.

“I was an avid bookworm, and I wanted that back. I was nervous, excited, all those things. There was no pain during the operation, but you’re still aware of what’s happening. It’s a new way of looking through your eyes, and it was dead exciting when I began seeing a letter. It’s not simple, learning to read again, but the more hours I put in, the more I pick up.

“The team at Moorfields has given me challenges, like ‘Look at your prescription’, which is always tiny. I like stretching myself, trying to look at the little writing on tins, doing crosswords.

“It’s made a big difference. Reading takes you into another world, I’m definitely more optimistic now.”

The global trial was led by Dr Frank Holz of the University of Bonn, with participants from the UK, France, Italy and the Netherlands.

The PRIMA System device used in this operation is being developed by Science Corporation (science.xyz), which develops brain-computer interfaces and neural engineering.

Mr Muqit added: “My feeling is that the door is open for medical devices in this area, because there is no treatment currently licensed for dry AMD – it doesn’t exist.

“I think it’s something that, in future, could be used to treat multiple eye conditions.”

More about the device:

The device is a novel wireless subretinal photovoltaic implant paired with specialised glasses that project near-infrared light to the implant, which acts like a miniature solar panel.

It is 30 micrometres/microns (0.03mm) thick, about half the thickness of a human hair.

A zoom feature gives patients the ability to magnify letters. It is implanted in the subretinal layer, under the retinal cells that have died. Until the glasses and waistband computer are turned on, the implant has no visual stimulus or signal to pass through to the brain.

In addition to practising their reading and attending regular training, patients on the trial were encouraged to explore ways of using the device. Sheila chose to learn to do puzzles and crosswords while one of the French patients used them to help navigate the Paris Metro – both tasks being more complex than reading alone.

Source: University College London

Categories : Implants and Prostheses OphthalmologyTags :

Oxford Researchers Develop Uniquely Shaped Microstent to Combat Glaucoma

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A schematic of the eye’s anterior segment, demonstrating the anatomical placement of the microstent. The stent diverts aqueous humour from the anterior chamber to the suprachoroidal space through the flexible tube, creating a subconjunctival bleb supported by the expanding element. Credit: Yunlan Zhang, Zhong You, Jared Ching.

A team of researchers at the University of Oxford have unveiled a pioneering ‘microstent’ which could revolutionise treatment for glaucoma, a common but debilitating condition. The study has been published in The Innovation, Cell Press.

Glaucoma is a leading cause of vision loss, second only to cataracts. Globally, 7.7 million people were blind or visually impaired due to glaucoma in 2020. The condition can cause irreversible damage to the optic nerve, due to increased pressure within the eyeball. Current treatment options – principally surgery to create openings in the eye or insert tubes to drain fluid – are highly invasive, carry risk of complications, and have limited durability.

‘Our deployable microstent represents a significant advancement in glaucoma treatment,’ said lead author Dr Yunlan Zhang (University of Oxford at the time of the study/University of Texas). ‘Current surgical implants for this type of glaucoma have been shown to have limited long-term effectiveness, being susceptible to failure due to fibrosis (scarring) in the eye.’ 

The new microstent features a unique structural shape that allows it to expand once in the eye. At 200µm, less than a quarter of a millimetre, the stent’s tiny diameter enables it to fit within the needle of a standard hypodermic syringe, for minimally-invasive insertion. Once in place and expanded, the microstent spans the fluid-filled space between the white of the eye and the membrane that covers it.

By supporting this space, the stent reduces the excessive fluid buildup and resulting intraocular pressure in the eye which is responsible for the most common type of glaucoma, primary open-angle glaucoma. Initial trials carried out in rabbits found that the microstents lowered eye pressure in less than a month with minimal inflammation and scarring. Furthermore, the microstent achieved a greater reduction of eye pressure than a standard tubular implant.

This development has the potential to transform the landscape of glaucoma therapy. By offering an enhanced solution in the minimally invasive glaucoma surgery field that combines mechanical innovation with biocompatibility, we hope to improve patient outcomes and quality of life.

Senior co-author Dr Jared Ching (Department of Engineering Science, University of Oxford).

Senior co-author, Professor Zhong You (Department of Engineering Science, University of Oxford) said: ‘Our microstent is made from a durable and super-flexible nickel-titanium alloy called nitinol, renowned for its proven long-term safety for ocular use. Its unique material and structural properties help prevent subsequent movement, improve durability, and ensure long-term efficacy.’

The research team used advanced modelling techniques to guide the microstent’s design and ensure compatibility with the anatomy of the eye. The device’s superelastic properties enable it to accommodate how the eye changes and stretches over time without permanent deformation, enhancing its durability and functionality.

Over half a million people in the UK have glaucoma – 2% of everyone over the age of 40 – and it is one of the most common causes of blindness worldwide. The introduction of this microstent could mark a pivotal step in enhancing treatment efficacy and accessibility.

The study ‘A Novel Deployable Microstent for the Treatment of Glaucoma has been published in The Innovation, Cell Press.

Source: Oxford University

Categories : OphthalmologyTags :

Blinking and Eyelid Function Is Enabled by Complex Control of Muscles

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Discovery could help pave the way for a prosthetic device to restore blink function lost to injury or disease

Muscle activation and movement patterns over time across the upper and lower eyelids, shown under different actions. Credit: Anatomical Engineering Group/UCLA

A blink of an eye is vital to protecting the eye by keeping it from drying out. This simple function seems natural and instantaneous, but is it?

Now, a team of UCLA biomechanical engineers and ophthalmologists has uncovered new details about the muscle that controls blinking, offering a pathway toward developing blink-assisting prostheses. Published in PNAS, the study found that the orbicularis oculi – the muscle that controls eyelid movement – contracts in complex patterns that vary by action and move the eyelid in more than just a simple up-and-down motion.

The researchers studied how this muscle behaves differently across various actions including spontaneous blinks, protective rapid closures and squeezed shut-eye motions.

“The eyelid’s motion is both more complex and more precisely controlled by the nervous system than previously understood,” said study corresponding author Tyler Clites, an assistant professor of mechanical and aerospace engineering at the UCLA Samueli School of Engineering. “Different parts of the muscle activate in carefully timed sequences depending on what the eye is doing. This level of muscle control has never been recorded in the human eyelid. Now that we have this information in rich detail, we can move forward in designing neuroprostheses that help restore natural eyelid function.”

In experiments with volunteers, the researchers looked at five different ways the eyes close:

  • Spontaneous blink: An automatic, unconscious blink that occurs regularly to keep the eye lubricated
  • Voluntary blink: An intentional blink, as when someone is asked to blink on command
  • Reflexive blink: A rapid, involuntary blink triggered to protect the eye from a collision
  • Soft closure: A gentle, slow eyelid descent, similar to the beginning of sleep
  • A forced closure: A deliberate squeezing of the eyelids tightly shut

To record activity in the orbicularis oculi with high precision, an ophthalmic surgeon inserted tiny wire electrodes into the eyelid. The researchers then used a motion-capture system to track eyelid movement in ultraslow motion. These tools allowed the team to measure subtle differences in eyelid movement, including speed, direction, and which part of the muscle initiated the action.

Video of spontaneous blink – dynamic muscle activation patterns and eyelid kinematics. Credit: Anatomical Engineering Group/UCLA

“People can lose the ability to blink due to a stroke, tumour, infection or injury. The condition is painful in the short term and can damage the eyes enough to cause vision loss,” said study co-author Dr Daniel Rootman, an associate professor of ophthalmology at the David Geffen School of Medicine at UCLA and director of the UCLA Orbital Disease Center. “We know that a small electric pulse can stimulate the orbicularis oculi muscle to move, but designing one that works well has been elusive. What we now have is a good roadmap to such a device, including where exactly to place electrodes, how to time them, and how strong the pulse should be. These guidelines could help pave the way for the development and clinical testing of such a device, with the ultimate goal of providing real relief for patients.”

With this fundamental knowledge of eyelid biomechanics in hand, the researchers can now work on refining a prototype neuroprosthesis to assist people with blinking.

“Understanding how the eyelid works is crucial to designing an accurate stimulation pattern for a prosthesis, as well as for diagnostic purposes,” said study first author Jinyoung Kim, a UCLA mechanical engineering doctoral student and member of Clites’ research group, the Anatomical Engineering Group at UCLA. “We are more than excited to bridge this gap and move forward to work with patients who have facial paralysis and help improve their lives.”

Source: UCLA Samueli School of Engineering

Categories : OphthalmologyTags :

Retinal Repair Work is Done by Microglia, not Neutrophils

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Findings have implications for understanding what goes wrong in retinal diseases

Photoreceptor cells in the retina. Credit: Scientific Animations

In a new study from the Flaum Eye Institute and Del Monte Institute for Neuroscience at the University of Rochester, researchers have discovered that the retina responds to damage differently than many other tissues in the body. When photoreceptor cells in the retina are damaged, microglia, or the brain’s immune cells, respond, and the neutrophils are not recruited to help despite passing through nearby blood vessels.

“This finding has high implications for what happens for millions of Americans who suffer vision loss through loss of photoreceptors,” said Jesse Schallek, PhD, associate professor of Ophthalmology and senior author of the study published in eLife. “This association between two key immune cell populations is essential knowledge as we build new therapies that must understand the nuance of immune cell interactions.”

Using adaptive optics imaging, a camera technology developed by the University of Rochester that allows the imaging of single neurons and immune cells inside the living eye, researchers studied the retinas of mice with photoreceptor damage. They found that while both neutrophil and microglia cells are present in the retina, only microglia cells respond to photoreceptor injury, and they do not call upon neutrophils to help repair the photoreceptor damage. Researchers believe this suggests a type of cloaking occurs during retinal injury to protect the retina from a rush of immune cells that could do more harm than good.

“What is remarkable here is that the passing neutrophils are so close to the reactive microglia, and yet they do not signal to them to assist in damage recovery,” said Schallek.

“This is notably different than what is seen in other areas of the body where neutrophils are the first to respond to local damage and mount an early and robust response.”

Source: University of Rochester Medical Center

Categories : New Compounds and Treatments OphthalmologyTags :

Boosting Apolipoprotein-M May Block Age-related Macular Degeneration

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Retina showing reticular pseudodrusen. Although they can infrequently appear in individuals with no other apparent pathology, their highest rates of occurrence are in association with age-related macular degeneration (AMD), for which they hold clinical significance by being highly correlated with end-stage disease sub-types, choroidal neovascularisation and geographic atrophy. Credit: National Eye Institute

A new study from Washington University School of Medicine in St. Louis identifies a possible way to slow or block progression of age-related macular degeneration, a leading cause of blindness in people over age 50. The WashU Medicine researchers and their international collaborators implicated problems with cholesterol metabolism in this type of vision loss, perhaps helping to explain the links between macular degeneration and cardiovascular disease, which both worsen with age.

The new findings, using human plasma samples and mouse models of macular degeneration, suggest that increasing the amount of a molecule called apolipoprotein M (ApoM) in the blood fixes problems in cholesterol processing that lead to cellular damage in the eyes and other organs. Various methods of dialing up ApoM could serve as new treatment strategies for age-related macular degeneration and perhaps some forms of heart failure triggered by similar dysfunctional cholesterol processing.

The study appears June 24 in the journal Nature Communications.

“Our study points to a possible way to address a major unmet clinical need,” said senior author Rajendra S. Apte, MD, PhD, professor of ophthalmology and visual sciences at WashU Medicine. “Current therapies that reduce the chance of further vision loss are limited to only the most advanced stages of macular degeneration and do not reverse the disease. Our findings suggest that developing treatments that increase ApoM levels could treat or even prevent the disease and therefore preserve people’s vision as they age.”

In macular degeneration, doctors can see cholesterol-rich deposits under the retina during an eye exam, according to Apte. In early stages, vision might still be normal, but the deposits increase inflammation and other damaging processes the lead to the gradual loss of central vision. In the most common type, “dry” macular degeneration, the cells in the central part of the retina can be damaged, causing a type of neurodegeneration called geographic atrophy, which is similar to what happens in the brain in conditions such as Alzheimer’s disease. Dry macular degeneration can turn into “wet” macular degeneration, in which abnormal blood vessel growth damages vision.

Geographic atrophy and wet macular degeneration are advanced forms of the disease that are accompanied by vision loss. Although some approved therapies for advanced disease are available, the disease process itself is not reversible at that stage.

A common culprit in eye disease and heart failure

In recent years, evidence has emerged that ApoM can serve as a protective molecule with known anti-inflammatory effects and roles in maintaining healthy cholesterol metabolism. With that in mind, Apte and co-senior author Ali Javaheri, MD, PhD, an assistant professor of medicine, were interested in assessing whether reduced ApoM levels, which fall with age, could be involved in the dysfunctional cholesterol metabolism that is at the root of multiple diseases of aging, including macular degeneration and heart disease. They showed that patients with macular degeneration have reduced levels of ApoM circulating in the blood compared with healthy controls. And past work by Javaheri, a WashU Medicine cardiologist, showed that patients with various forms of heart failure also had reduced levels of ApoM in the blood.

This study revealed that ApoM is a key component in the “good cholesterol” pathways that mop up excess “bad” LDL cholesterol and excrete it via the liver.

Apte and Javaheri’s research suggests that when ApoM is low, cells in the retina and heart muscle can’t correctly metabolise cholesterol deposits and struggle to clear these accumulating lipids. When these lipids build up, it leads to inflammation and cellular damage.

To see if they could reverse the harmful effects of low ApoM, the researchers increased ApoM levels in mouse models of macular degeneration, using genetic modification or plasma transfer from other mice. The mice showed evidence of improved retinal health, improved function of light-sensing cells in the retina and reduced accumulation of cholesterol deposits. The researchers further found evidence that ApoM triggers a signalling pathway that breaks down the cholesterol in cellular compartments called lysosomes, which are known for playing important roles in disposing of cellular waste.

The researchers also found that ApoM must be bound to a molecule called sphingosine-1-phosphate (S1P) to get the beneficial effects of ApoM treatment in the mice.

The findings also could have implications for future interventions that raise ApoM in patients with heart failure.

“One of the exciting things about this collaboration is realising the links between retinal pigment epithelial cells and heart muscle cell, which are both vulnerable to low ApoM,” Javeheri said. “It is possible that the interaction between ApoM and S1P is regulating cholesterol metabolism in both cell types. We look forward to exploring strategies to increase ApoM in ways that could help the eye and the heart maintain healthy cholesterol metabolism over time and stave off two major diseases of aging.”

Source: WashU Medicine

Categories : Diet and Nutrition OphthalmologyTags :

Vitamin Supplements Slow Down the Progression of Glaucoma

On By Peter Van Dyk
Photo by Ksenia Chernaya

A vitamin supplement that improves metabolism in the eye appears to slow down damage to the optic nerve in glaucoma. Promising results have been published in the journal Cell Reports Medicine. The researchers behind the study have now started a clinical trial on patients.

In glaucoma, the optic nerve is gradually damaged, leading to vision loss and, in the worst cases, blindness. High pressure in the eye drives the disease, and eye drops, laser treatment or surgery are therefore used – with varying effect – to lower the pressure in the eye and thus slow down the disease.

Glaucoma researchers have long theorised that the substance homocysteine is somehow relevant to understanding the disease. Now, researchers at Karolinska Institutet have investigated the role of homocysteine in several ways. In the current study, the researchers discovered that when rats with glaucoma were given elevated levels of homocysteine, their disease did not worsen. 

Investigated metabolic pathways

The researchers also found that high levels of homocysteine in the blood of people with glaucoma did not correlate with how quickly the disease progressed, and that glaucoma was not more common in people with a genetic susceptibility to forming high levels of homocysteine. Based on these findings, the researchers concluded that homocysteine does not drive the disease but is a consequence of it.

Since homocysteine is a natural part of the body’s metabolism, the researchers wanted to investigate metabolic pathways involving homocysteine in both rodents and humans with glaucoma. They then saw several abnormalities, the most important of which were metabolic changes linked to the retina’s ability to use certain vitamins. This change meant that metabolism was slowed down locally in the retina – and this played a role in the development of the disease. 

“Our conclusion is that homocysteine is a bystander in the disease process, not a player. Altered homocysteine levels may reveal that the retina has lost its ability to use certain vitamins that are necessary to maintain healthy metabolism. That’s why we wanted to investigate whether supplements of these vitamins could protect the retina”, says co-lead on the paper James Tribble, researcher and assistant professor at the Department of Clinical Neuroscience at Karolinska Institutet.

Promising results lead to clinical trial

In experiments on mice and rats with glaucoma, the researchers gave supplements of the B vitamins B6, B9 and B12, as well as choline. This had a positive effect. In mice that had a slower developing glaucoma, the damage to the optic nerve was completely halted. In rats, which had a more aggressive form of the disease with faster progression, the disease was slowed down. 

In these experiments, eye pressure was left untreated, which the researchers highlight as particularly interesting – it suggests that the vitamin mix affects the disease in a different way than lowering eye pressure does. 

“The results are so promising that we have started a clinical trial, with patients already being recruited at S:t Eriks Eye Hospital in Stockholm”, says James Tribble. 

Both patients with primary open-angle glaucoma (slower progression) and pseudoexfoliation glaucoma (faster progression) are included. 

Read more about the clinical trial here. 

Source: Karolinska Institutet

Categories : OphthalmologyTags :

The Rise in Dry Eye Disease Among Young Adults

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Photo by Steinar Engeland on Unsplash

Researchers at Aston University have called for more advice to be given to young people about preventing dry eye disease, after a study carried out in conjunction with Oslo University Hospital and Sørlandet Hospital Trust in Norway found that 90% of participants had at least one sign of the condition in their eyes.

Dry eye disease occurs when the eyes do not make enough tears, or make poor-quality tears without sufficient lipid or mucus levels which leads to poor tear film stability and rapid evaporation. Sufferers may have gritty feeling eyes, itching or stinging in the eyes, red eyes, sensitivity to light and blurry vision. There are several risk factors for dry eye disease, including stress and wearing contact lenses. It is also more prevalent in females. In the 18-25 age group, a major risk factor is screen use.

The research, following 50 18-25-year-olds over time, was led by Dr Rachel Casemore at Aston University School of Optometry and is the first of its kind. It was published in The Ocular Surface. The researchers looked for symptoms of dry eye disease in the participants, studied lifestyle factors, and followed up with participants one year on to find out if there had been any progression of the condition.

The initial study showed that 56% of participants had dry eye disease, while 90% had at least one symptom of the condition. Around half of the participants in the study had lost at least 25% of a type of gland in the eye called the meibomian gland. These glands produce the outer lipid layer of the eye’s tear film, which is responsible for preventing evaporation of tears, and therefore keeps the tear film stable and the eye moist. One year on, the researchers found that there had been significant progression of dry eye disease in the study participants.

Additionally, the researchers found correlation found between how long the study group used screens and signs of dryness on the eye surface. The average screen use of participants was eight hours per day.

The researchers concluded that the evidence of dry eye disease symptoms and progression in the young adults in their study shows the need for early detection of potential signs, and the identification of those who may go on to develop dry eye disease. These individuals can then be advised on managing the condition before progression.

The progression and development of dry eye disease can be slowed by various methods. Dr Casemore says that the simplest ways are to take regular screen breaks, to carry out blink exercises to ensure the release of oils from the meibomian glands and to keep hydrated. A healthy, balanced diet, including sources of omega-3 fatty acids, such as oily fish, is also important, as is regular sleep patterns.

Dr Casemore suggests that those with irregular sleep patterns, such as those caused by sleep disorders or anxiety, should seek advice. People who wear contact lenses need to ensure they get regular check-ups to ensure optimum fitting, and that they adhere to their replacement schedule, wearing time schedule, cleaning regimes and safety advice, such as no sleeping, showering or swimming in contact lenses.

Dr Casemore said:

“It is concerning to note the increasing prevalence of dry eye disease signs and symptoms in young adults, which has been referred to as a ‘lifestyle epidemic’ by some researchers. Eye care practitioners are well placed to identify the clinical indicators of dry eye disease and counsel young adults around modifiable risk factors, such as screen use habits, sleeping habits, contact lens use, diet, blinking patterns, and management of stress levels.

“Our future research aims to continue investigation of the potential tear and meibomian gland oil biomarkers which were identified during the study and further explore the effect of diet on dry eye disease development.”

Source: Aston University

Categories : Mental Health OphthalmologyTags :

Genetic Schizophrenic Susceptibility Could Show up in the Retina

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Photoreceptor cells in the retina. Credit: Scientific Animations

Could the eyes, which are directly connected to the brain, hold clues to brain changes? An international team of researchers led by the University of Zurich and the University Hospital of Psychiatry Zurich has now tackled this very question. In their study, published in Nature Mental Health, the researchers examined whether changes in our nerve connections are linked to a genetic risk for schizophrenia, as impaired neural information processing is one of the main characteristics of the disorder.

Previous studies suggest that schizophrenia not only reduces volume of grey matter in the brains of those affected, but that it also leads to loss of retinal tissue. But whether these changes are the cause of schizophrenia or a consequence of the disorder has remained unanswered. Retinal health could also be affected by schizophrenia itself, for example, through antipsychotic medication, lifestyle factors or diabetes.

Extensive use of data from healthy individuals

“To investigate whether the risk of developing schizophrenia has an effect on the central nervous system, we examined tens of thousands of healthy individuals,” says Finn Rabe, first author of the study and postdoc at the University of Zurich. “We then calculated polygenic risk scores for each individual.”

The researchers were able to use extensive genetic and retinal data taken from the UK Biobank, a large biomedical database containing data from over half a million people. “You could say that the scale of the UK Biobank’s data has revolutionised biomedical research,” the researcher adds.

Thin retina, elevated risk

The study shows that higher genetic susceptibility to schizophrenia is indeed associated with thinner retinas. The effects are small, though, and can only be reliably demonstrated in large-scale studies. One of the study’s findings is that, unlike changes in the brain, changes in the retina are easy to detect using non-invasive and inexpensive retinal measurements. Thanks to optical coherence tomography, which can be described as a kind of ultrasound for the eye, retinal thickness can be measured in minutes.

This offers a promising outlook for prevention. “Our study shows the potential of using optical coherence tomography in clinical practice. But large-scale longitudinal studies are needed to examine how useful it will be for prevention,” says Finn Rabe.

Perspectives for new therapies

Another key finding of the study concerns genetic variants associated with inflammatory processes in the brain. These may also contribute to structural changes in the retina. The study thus offers further support for the inflammation hypothesis of schizophrenia, ie, the idea that inflammatory processes contribute to the development or progression of the disorder. “If this hypothesis is confirmed, inflammation could be interrupted by medication, potentially enabling us to improve treatment possibilities in the future,” says Rabe.

Source: University of Zurich