blindness Archives - Amazing Health Advances

Toxic DNA Buildup in Eyes With Macular Degeneration Can Cause Blindness – Study

AHA Publisher — Fri, 08 Oct 2021 07:00:09 +0000

Jerusalem Post Staff via The Jerusalem Post – Scientists have discovered a buildup of damaging DNA in the eyes of patients with macular degeneration, which in turn could cause blindness. This new research comes from the University of Virginia School of Medicine and was published in the journal Science Advances. Scientists have suggested, according to their research, that common HIV drugs may help stop vision loss. The harmful DNA that is a threat to one’s eyes is referred to as the Alu DNA. According to the researchers, these new findings offer insights into how geographic atrophy progresses over time. “Although we’ve known that geographic atrophy expands over time, we didn’t know how or why,” said Ambati, of UVA’s Department of Ophthalmology and Center for Advanced Vision Science. Macular degeneration affects around 200 million people worldwide. Geographic atrophy is age-related and destroys the light-sensing portion of the eye. Ambati, a top expert in macular degeneration, discovered that this destruction is caused by the buildup of Alu DNA. Ambati concluded that Alu DNA triggers inflammation in the eye, which can be combated with HIV drugs such as nucleoside or NRTIs. Researchers discovered this by testing the drugs on lab mice.“Our findings from human eyes show that these toxic molecules, which activate the inflammasome, are most abundant precisely in the area of greatest disease activity,” Ambati said. To read the original article click here.

The post Toxic DNA Buildup in Eyes With Macular Degeneration Can Cause Blindness – Study appeared first on Amazing Health Advances.

Vision Impairment Is Associated With Mortality

AHA Publisher — Fri, 19 Mar 2021 07:00:08 +0000

Michigan Medicine – University of Michigan via EurekAlert – The global population is aging, and so are their eyes. In fact, the number of people with vision impairment and blindness is expected to more than double over the next 30 years. A meta-analysis in The Lancet Global Health, consisting of 48,000 people from 17 studies, found that those with more severe vision impairment had a higher risk of all-cause mortality compared to those that had normal vision or mild vision impairment. According to the data, the risk of mortality was 29% higher for participants with mild vision impairment, compared to normal vision. The risk increases to 89% among those with severe vision impairment. Importantly, four of five cases of vision impairment can be prevented or corrected. Globally, the leading causes of vision loss and blindness are both avoidable: cataract and the unmet need for glasses. The study’s lead author, Joshua Ehrlich, M.D., M.P.H., sought to better understand the association between visual disabilities and all-cause mortality. The work compliments some of Ehrlich’s recent research, also in The Lancet Global Health Commission on Global Eye Health, that highlighted the impact of late-life vision impairment on health and well-being, including its influence on dementia, depression, and loss of independence. “It’s important these issues are addressed early on because losing your vision affects more than just how you see the world; it affects your experience of the world and your life,” says Ehrlich. “This analysis provides an important opportunity to promote not only health and wellbeing, but also longevity by correcting, rehabilitating, and preventing avoidable vision loss across the globe.” To read the original article click here.

The post Vision Impairment Is Associated With Mortality appeared first on Amazing Health Advances.

Could a Tiny Fish Hold the Key to Curing Blindness?

AHA Publisher — Wed, 30 Sep 2020 07:00:45 +0000

NIH, National Eye Institute (NEI) via Newswise – Imagine this: A patient learns that they are losing their sight because an eye disease has damaged crucial cells in their retina. Then, under the care of their doctor, they simply grow some new retinal cells, restoring their vision. Although science hasn’t yet delivered this happy ending, researchers are working on it – with help from the humble zebrafish. When a zebrafish loses its retinal cells, it grows new ones. This observation has encouraged scientists to try hacking the zebrafish’s innate regenerative capacity to learn how to treat human disease. That is why among the National Eye Institute’s 1,200 active research projects, nearly 80 incorporate zebrafish. The retina is a layer of tissue in the back of the eye that responds to light. But many scientists think of the retina as part of the brain. Like other neurons of the central nervous system, retinal neurons typically don’t replicate in adult humans. Loss of retinal neurons typically results in irreversible vision loss. Image credit: National Eye Institute However, zebrafish, like newts, frogs, and a strange fish-like salamander called the axolotl, can regrow a variety of body parts – not only retinal neurons, but also the heart, fins, pancreas, brain, spinal cord, and kidney. Zebrafish have a variety of traits that make them a great model for studying tissue regeneration: They’re capable of reproducting hundreds of offspring at a time. They’re cheap to maintain and express about 70% of the same genes that humans do. Unlike mice, which develop in a womb, zebrafish develop externally where scientists can easily observe them. And their flesh is nearly transparent during development, enabling researchers to observe their internal organs. Scientists have long known that when zebrafish retinas are damaged, neuronal support cells called Müller glia start dividing to create neuronal precursor cells, which go on to become replacement retinal neurons. More recently, scientists have been trying to unravel the biological factors that initiate this process. Progress in that effort is detailed in several NEI-supported research projects over the past three years. Studying zebrafish, James Patton of Vanderbilt University and colleagues found that when levels of the neurotransmitter GABA decrease, neural stem cells activate. These cells then migrate to damaged retina and develop (differentiate) into whatever cell type is needed for repair. Patton’s findings help identify cues that stimulate zebrafish regeneration. Jeff Mumm, Johns Hopkins University, reported that immune cells in the retina called microglia are necessary for zebrafish Müller glia to initiate regeneration after injury. After selectively knocking out microglia with a toxic enzyme, Mumm found that the Müller glia showed almost no regenerative activity after three days of recovery, compared with approximately 75 percent regeneration in control zebrafish. However, when an immunosuppressant was applied to inhibit microglia reactivity a day after retinal cell loss had begun, the pace of retinal neuron replacement accelerated. This observation suggests that microglia play different roles at different stages of injury/regeneration. Jeff Mumm, Johns Hopkins, and collaborators, fluorescently labeled immune cells in zebrafish larvae to track immune system activity in a model of retinal degeneration. Image credit: Credit: David White, Mumm Lab, Johns Hopkins University School of Medicine Findings in zebrafish by these other groups led Tom Reh at the University of Washington to unlock the regenerative potential of cells in the mouse retina. In newborn mice, the gene regulatory factor Ascl1 can direct Muller glia to become retinal neurons. This gene goes dormant when mice mature. By artificially expressing the Ascl1 gene in adult mouse Muller glia, Reh’s team turned the gene program back on, showing for the first time that Müller glia in the adult mouse can give rise to new functional neurons after injury. These neurons have the gene expression pattern, the morphology, the electrophysiology, and the epigenetic program to look like interneurons instead of glia, according to the report, and connect with the existing retinal circuitry and respond to light. A second major challenge of regenerating the visual system is figuring out how replacement neurons in zebrafish find their way back to visual centers of the brain. The light-sensing photoreceptors connect to retinal ganglion cells (RGCs). RGC cell fibers called axons coalesce within the optic nerve where they exit the eye and disperse throughout the brain. Beth Harvey, a postdoctoral researcher working with Michael Granato at the University of Pennsylvania, has developed a model for studying this process.1 She uses zebrafish at the late larval stage so that she can observe RGC axons navigate to their appropriate brain target after injury, using a technique called confocal microscopy. Interestingly, she found that axons are more likely to innervate appropriate targets when the optic nerve is only partially cut—like leaving a trail of breadcrumbs for regenerating axons to follow. Illustration of zebrafish head showing optic nerve, eye, and brain. Image courtesy of Beth Harvey, University of Pennsylvania. To accelerate progress, the NEI funded a consortium of scientists as part of its Audacious Goals Initiative to identify biological factors that affect the restoration of functional connections within the retina and between the eye and brain. Projects within the consortium have used various models to evaluate hundreds of genes for their role in regeneration as well as compounds that modify their activity. In partnership with Michael Dyer from St. Jude’s Children’s Hospital, the NEI is uploading consortium data to an online database to help future investigations. References 1. Harvey, B. M., Baxter, M. & Granato, M. Optic nerve regeneration in larval zebrafish exhibits spontaneous capacity for retinotopic but not tectum specific axon targeting. PLoS One 14, e0218667, doi:10.1371/journal.pone.0218667 (2019). To read the original article click here.

The post Could a Tiny Fish Hold the Key to Curing Blindness? appeared first on Amazing Health Advances.

Researchers Discover Stem Cells in Optic Nerve That Preserve Vision

AHA Publisher — Fri, 31 Jul 2020 07:00:03 +0000

University of Maryland School of Medicine via EurekAlert – Researchers at the University of Maryland School of Medicine (UMSOM) have for the first time identified stem cells in the region of the optic nerve, which transmits signals from the eye to the brain. The finding, published this week in the journal Proceedings of the National Academy of Sciences (PNAS), presents a new theory on why the most common form of glaucoma may develop and provides potential new ways to treat a leading cause of blindness in American adults. “We believe these cells, called neural progenitor cells, are present in the optic nerve tissue at birth and remain for decades, helping to nourish the nerve fibers that form the optic nerve,” said study leader Steven Bernstein, MD, PhD, Professor and Vice Chair of the Department of Ophthalmology and Visual Sciences at the University of Maryland School of Medicine. “Without these cells, the fibers may lose their resistance to stress, and begin to deteriorate, causing damage to the optic nerve, which may ultimately lead to glaucoma.” The study was funded by the National Institutes of Health’s National Eye Institute (NEI), and a number of distinguished researchers served as co-authors on the study. More than 3 million Americans have glaucoma, which results from damage to the optic nerve, causing blindness in 120,000 U.S. patients. This nerve damage is usually related to increased pressure in the eye due to a buildup of fluid that does not drain properly. Blind spots can develop in a patient’s visual field that gradually widen over time. “This is the first time that neural progenitor cells have been discovered in the optic nerve. Without these cells, the nerve is unable to repair itself from damage caused by glaucoma or other conditions. This may lead to permanent vision loss and disability,” said Dr. Bernstein. “The presence of neural stem/progenitor cells opens the door to new treatments to repair damage to the optic nerve, which is very exciting news.” To make the research discovery, Dr. Bernstein and his team examined a narrow band of tissue called the optic nerve lamina. Less than 1 millimeter wide, the lamina lies between the light-sensitive retina tissue at the back of the eye and the optic nerve. The long nerve cell fibers extend from the retina through the lamina, into the optic nerve. What the researchers discovered is that the lamina progenitor cells may be responsible for insulating the fibers immediately after they leave the eye, supporting the connections between nerve cells on the pathway to the brain. The stem cells in the lamina niche bathes these neuron extensions with growth factors, as well as aiding in the formation of the insulating sheath. The researchers were able to confirm the presence of these stem cells by using antibodies and genetically modified animals that identified the specific protein markers on neuronal stem cells. “It took 52 trials to successfully grow the lamina progenitor cells in a culture,” said Dr. Bernstein, “so this was a challenging process.” Dr. Bernstein and his collaborators needed to identify the correct mix of growth factors and other cell culture conditions that would be most conducive for the stem cells to grow and replicate. Eventually the research team found the stem cells could be coaxed into differentiating into several different types of neural cells. These include neurons and glial cells, which are known to be important for cell repair and cell replacement in different brain regions. This discovery may prove to be game-changing for the treatment of eye diseases that affect the optic nerve. Dr. Bernstein and his research team plan to use genetically modified mice to see how the depletion of lamina progenitor cells contributes to diseases such as glaucoma and prevents repair. Future research is needed to explore the neural progenitors repair mechanisms. “If we can identify the critical growth factors that these cells secrete, they may be potentially useful as a cocktail to slow the progression of glaucoma and other age-related vision disorders.” Dr. Bernstein added. The work was supported by NEI grant RO1EY015304, and by a National Institutes of Health shared instrument grant 1S10RR26870-1. “This exciting discovery could usher in a sea change in the field of age-related diseases that cause vision loss,” said E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. “New treatment options are desperately needed for the millions of patients whose vision is severely impacted by glaucoma, and I think this research will provide new hope for them.” To read the original article click here.

The post Researchers Discover Stem Cells in Optic Nerve That Preserve Vision appeared first on Amazing Health Advances.

Low-Carbohydrate Diet May Be Associated With Lower Risk of Blinding Eye Disease

AHA Publisher — Fri, 17 Jul 2020 07:00:19 +0000

Mount Sinai Health System via Newswise – Following a long-term diet that’s low in carbohydrates and high in fat and protein from vegetables may lower the risk of the most common subtype of glaucoma. In a first-of-its-kind study, a researcher at New York Eye and Ear Infirmary of Mount Sinai (NYEE) helped discover that if at-risk groups adhere to these dietary restrictions, they may reduce their risk of developing primary open angle glaucoma with early paracentral visual loss by 20 percent. Results from the research have been published in the July 22 issue of Eye-Nature. The study is important because glaucoma is the leading cause of blindness in the United States and primary open angle glaucoma (POAG) is the most common type. POAG is the leading cause of optic nerve degeneration that is related to the pressure level inside the eye, but other factors also contribute to this condition. Patients typically experience few or no symptoms until the disease progresses and they have vision loss. “A diet low in carbohydrates and higher in fats and proteins results in the generation of metabolites favorable for the mitochondrion-rich optic nerve head, which is the site of damage in POAG. This dietary pattern has already been shown to have favorable results for epilepsy and showed some promising results for Parkinson’s and Alzheimer’s diseases,” said co-corresponding author Louis R. Pasquale, MD, FARVO, Deputy Chair for Ophthalmology Research for the Mount Sinai Health System. “It’s important to note that a low-carbohydrate diet won’t stop glaucoma progression if you already have it, but it may be a means to preventing glaucoma in high-risk groups. If more patients in these high-risk categories—including those with a family history of glaucoma—adhered to this diet, there might be fewer cases of vision loss.” Past studies have shown that a ketogenic diet (low-carbohydrate and high-fat) has a protective effect against neurologic disorders. Ketone bodies (energy compounds produced as the body metabolizes fats) are substituted for glucose as a major energy source for the brain and using more of these under a ketogenic diet may improve function and slow down neuronal degeneration. However, more recent studies have shown that a low-carbohydrate diet that does not restrict protein or total calories may have similar neuroprotective properties; this diet has been recognized as a more practical alternative to a ketogenic diet, as it’s easier to follow and does not have the adverse effects of the ketogenic diet (which range from headache, weakness, and irritability to constipation, nausea, and vomiting). A team of researchers wanted to know if a low-carbohydrate diet could positively impact the optic nerve. The optic nerve sits in the back of the eye and transfers visual information from the retina to the brain through electrical impulses. The optic nerve has a large concentration of mitochondria (mitochondria represent the major source of a cell’s energy supply and lead to a cell’s survival), and has high-energy requirements. Since glaucoma is a condition that may be associated with mitochondrial dysfunction, researchers wanted to find out if substituting protein and fat for carbohydrates in the diet would enhance mitochondrial activity, maintain optic nerve function, and prevent optic nerve degeneration in this blinding eye disease. They performed a large-scale meta-analysis to get this answer. They followed 185,000 adult participants from three large studies in the United States, conducted between 1976 and 2017. Participants were female nurses and male health professionals between the ages of 40 and 75. Every two to four years, they filled out food frequency questionnaires that assessed what they ate and drank. They also answered questions about their health and what diseases, if any, they might be developing. If they said they had glaucoma, the researchers asked their treating eye care providers to send medical records to determine if they had POAG. The research team created statistical models based on the patients’ questionnaire responses, dividing them into groups based on carbohydrate intake, so they could look across the spectrum from high to low carbohydrate intake and see any possible relationship with POAG. They specifically looked at three different ways of achieving a low-carbohydrate diet: substituting animal-based fats and proteins for carbohydrates; substituting plant-based based fats and proteins for carbohydrates; and replacing carbohydrates with high fats and proteins regardless of the source. Researchers then calculated the relative risk of POAG after adjusting for multiple factors for each of the dietary patterns including age, race, and body mass index. Patients in the low-carbohydrate intake group who followed a diet of increased plant-based fat and protein were associated with a 20 percent lower risk of developing POAG subtype with paracentral visual field loss compared to those in the high-carbohydrate intake group. However, the researchers did not find any association between POAG and a low-carbohydrate diet without accounting for the source protein or fat, and they did not find any association between glaucoma and an animal-based low-carbohydrate diet. Their findings suggest vegetable sources may be more beneficial than animal sources for a low-carbohydrate diet with respect to reducing risk of the specific glaucoma subtype with early paracentral visual loss. “This was an observational study and not a clinical trial, so more work is needed as this is the first study looking at this dietary pattern in relation to POAG. The next step is to use artificial intelligence to objectively quantify paracentral visual loss in our glaucoma cases and repeat the analysis,” adds Dr. Pasquale. “It’s also important to identify patients who have a genetic makeup of primary open angle glaucoma who may benefit from a low-carbohydrate diet. This dietary pattern may be protective only in people with a certain genetic makeup.” To read the original article click here.

The post Low-Carbohydrate Diet May Be Associated With Lower Risk of Blinding Eye Disease appeared first on Amazing Health Advances.

Electrical Stimulation Could Restore Vision in Blind People

AHA Publisher — Fri, 10 Jul 2020 07:00:40 +0000

University of Zurich via News-Medical Net – In a project under Horizon 2020, researchers from seven European organizations will examine how the vision of visually impaired people can be restored using electrical stimulation of the brain. The project is being coordinated by the University of Zurich and supported by the European Union with funding of 4 million euros. If a project receives funding from the European Union, it must involve excellent science in innovative and promising interdisciplinary research fields that provide new and relevant ideas for industry and society. The international Neural Active Visual Prosthetics for Restoring Function project meets all these criteria and has been awarded an EU research grant totaling 4 million euros over four years. The project will kick off on 1 September 2020 and is being coordinated by Prof. Shih-Chii Liu at the Institute of Neuroinformatics of the University of Zurich. Working in interdisciplinary teams from seven European universities and institutions with complementary expertise in computational, systems and clinical neuroscience, materials engineering, microsystems design, and deep learning, the project will develop technology to restore the vision of blind people through electrical stimulation of the brain. Close Interdisciplinary Cooperation The aim of the project is to develop a neuroprosthesis with thousands of electrodes driven by adaptive machine learning algorithms for a new brain-computer interfacing technology. “We want to create a novel neuroprosthesis system that is lightweight, robust and portable, and which will remain effective for decades,” explains Shih-Chii Liu. Current systems only stimulate a small set of neurons in the brain, and interfaces have longevity of only a few months. Liu is convinced that the project will succeed in its goals: “All the partners have long-time experience in their respective fields, so the required background knowledge is already in place. The breakthroughs will come with the planned larger-scale efforts and partner interactions in this project.” The challenge will be coordinating the expected breakthroughs across multiple disciplines. Establishing Innovation These breakthroughs include innovative approaches for stimulation with high-electrode-count interfacing with the visual cortex. For this, thin flexible probes are needed that cause minimal tissue damage as well as new electrode coatings and novel microchip methods. The researchers will also channel the stimulation currents to many thousands of electrodes and monitor neuronal activity in higher cortical areas. Breakthroughs are also expected when it comes to artificial neural networks trained by deep learning, which will only extract the most relevant visual information from a camera input to enable blind individuals to recognize objects and facial expressions and navigate through unfamiliar environments. These networks will transform the camera footage into stimulation patterns that drive the neurons in a way that the blind person can interpret. This is the only way that the signals can be processed and passed on. At the same time, eye tracking will be used to improve perception in a closed-loop approach. The Algorithm Translates Stimulation Patterns In addition to coordinating the project, the University of Zurich is also contributing to its technological expertise. The neuroinformatics team of Shih-Chii Liu and Tobi Delbruck will be working with consortium partners to develop power-efficient neuromorphic deep learning hardware and algorithms. The network implemented on the neuromorphic hardware will translate camera input into stimulation patterns to drive the stimulation electrodes. This research project is important because it lays ground-breaking work for constructing a new brain neuroprosthesis and brings added benefits to other neuroprosthesis research.” Shih-Chii Liu, Professor, Institute of Neuroinformatics, University of Zurich The involved researchers hope that the project will raise Europe’s still relatively low profile in this research field. To read the original article click here.

The post Electrical Stimulation Could Restore Vision in Blind People appeared first on Amazing Health Advances.

Shining a Light on How Exercise Reduces Cataract Risk

AHA Publisher — Mon, 22 Jun 2020 07:00:20 +0000

University of South Australia via Newswise– Chinese and Australian researchers have combined studies of more than 170,000 people and found conclusive evidence that regular physical exercise reduces the risk of age-related cataracts, the cause of blindness in an estimated 13 million people worldwide. In a recent paper published in the International Journal of Ophthalmology, researchers from Xi’an Jiaotong University and the University of South Australia (UniSA) analysed data from six different studies looking at how exercise reduces oxidative damage in the eye. The researchers found a 10 per cent reduction in age-related cataracts (ARC) among people who engaged in regular physical activity such as walking and cycling. UniSA epidemiologist Dr Ming Li says physical activity reduces oxidative stress in the eye by inhibiting lipid degradation which results in cell damage. “We know that exercise increases antioxidant enzyme activity which has all sorts of benefits, including limiting infections and inflammation in the eye,” Dr Li says. Previous studies have shown that long-term physical activity also elevates HDL (high-density lipoprotein), otherwise known as the ‘good cholesterol’, which may carry more antioxidants from plasma to the lens to prevent oxidative damage. Exercise also improves insulin resistance and lipid profiles, both of which have been associated with an increased risk of ARC. “Age-related cataracts are one of the most common causes of vision impairment and blindness in the world and although surgery is an effective option to recover vision, it is very costly,” Dr Li says. “The lens is highly susceptible to oxidative damage because of its high concentration of polyunsaturated fatty acid and its specific biological function. Although we don’t completely understand the mechanisms underlying ARC, we do know that ageing and oxidative damage play a crucial role in the development of the disease.” The researchers found that the risk of developing cataracts could potentially decrease by two per cent for every hour of cycling or walking per day. “Considering the fact that 24 per cent of adults are inactive, these findings will hopefully encourage older people to start exercising on a regular basis,” Dr Li says. To read the original article click here.

The post Shining a Light on How Exercise Reduces Cataract Risk appeared first on Amazing Health Advances.

Dynamic Stimulation of the Visual Cortex Allows Blind and Sighted People to ‘See’ Shapes

AHA Publisher — Fri, 15 May 2020 07:00:21 +0000

Cell Press via EurekAlert – For most adults who lose their vision, blindness results from damage to the eyes or optic nerve while the brain remains intact. For decades, researchers have proposed developing a device that could restore sight by bypassing damaged eyes and delivering visual information from a camera directly to the brain. In a paper publishing in the journal Cell on May 14, a team of investigators at Baylor College of Medicine in Houston report that they are one step closer to this goal. They describe an approach in which implanted electrodes are stimulated in a dynamic sequence, essentially “tracing” shapes on the surface of the visual cortex that participants were able to “see.” “When we used electrical stimulation to dynamically trace letters directly on patients’ brains, they were able to ‘see’ the intended letter shapes and could correctly identify different letters,” senior author Daniel Yoshor says. “They described seeing glowing spots or lines forming the letters, like skywriting.” Previous attempts to stimulate the visual cortex have been less successful. Earlier methods treated each electrode like a pixel in a visual display, stimulating many of them at the same time. Participants could detect spots of light but found it hard to discern visual objects or forms. “Rather than trying to build shapes from multiple spots of light, we traced outlines,” says first author Michael Beauchamp. “Our inspiration for this was the idea of tracing a letter in the palm of someone’s hand.” The investigators tested the approach in four sighted people who had electrodes implanted in their brains to monitor epilepsy and two blind people who had electrodes implanted over their visual cortex as part of a study of a visual cortical prosthetic device. Stimulation of multiple electrodes in sequences produced perceptions of shapes that subjects were able to correctly identify as specific letters. The approach, the researchers say, demonstrates that it could be possible for blind people to regain the ability to detect and recognize visual forms by using technology that inputs visual information directly into the brain, should they wish to. The researchers note, however, that several obstacles must be overcome before this technology could be implemented in clinical practice. “The primary visual cortex, where the electrodes were implanted, contains half a billion neurons. In this study we stimulated only a small fraction of these neurons with a handful of electrodes,” Beauchamp says. “An important next step will be to work with neuroengineers to develop electrode arrays with thousands of electrodes, allowing us to stimulate more precisely. Together with new hardware, improved stimulation algorithms will help realize the dream of delivering useful visual information to blind people.” To read the original article click here.

The post Dynamic Stimulation of the Visual Cortex Allows Blind and Sighted People to ‘See’ Shapes appeared first on Amazing Health Advances.