Sunday, January 05, 2020

Blindness in AMD patients: Study says brain can integrate artificial and natural vision correctly

A new research  has found that the brain knows how to integrate natural and artificial vision while maintaining information processing that is important for the vision which can help in better treatment for age-related macular degeneration (AMD).

The study mentioned that AMD in the West causes blindness in millions of people. In the Western world, it is the most common cause of serious vision loss for those aged 50 and over and is growing with age. Although no remedy is available for AMD, recent significant advances in artificial retina implants may contribute to effective treatment.

Locate inside the eye, the retina contains light receptors ( photo-receptors) that absorb light. Information is then processed and transmitted to the brain.

The macula, the central area of the retina, processes most of the information that reaches the brain from the eye. enabling one to see while reading and driving, facial recognition, and any other activity that required accurate vision.

In the peripheral retina, the area of the retina outside the macula that assist mainly with spatial judgement, vision is 10-20 times less precise.

in AMD, precise vision is impaired due to damage to the centre of the retina, while peripheral vision remains normal.

When there is damage to the photo-receptor layers in the retina, an artificial retina may be implanted. Activating these electrodes results in electrical stimulation of the remaining retina cells and results in the visual restoration, albeit partially.

AMD patients implanted with an artificial retina possess a combination of artificial central vision and normal peripheral vision. This combination of artificial and natural vision is important to study in order to understand how to help the blind.

One of the key issues here is whether the brain can integrate artificial and natural vision correctly.
One of the researchers has used a unique projection system that stimulated either natural vision, artistic vision or a combination of natural and artificial vision and at the same time records cortical responses in rodents implanted with a subretinal implant.

The implant is made up of dozens of small solar cells and electrodes developed at Standford Uni.
These ground breaking findings have implications on better vision restore for retinal prosthetic implanted in AMD patients and help the theory of incorporation of prosthetic and natural vision into the brain.
The findings can also have an impact on future brain-machine interface systems where artificial and natural procedures co-exist, said the Prof.

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Wednesday, September 06, 2017

This gene can cause vision loss in middle-age

According to researchers, chemical changes in the eye can lead to blindness in middle-age.

Their findings aid understanding of a genetic condition that causes sight loss for one in 3,000 people.


The team examined how changes in a gene - known as RPGR - can damage eye cells to cause a disorder known as X-linked retinitis pigmentosa - a chronic hereditary eye disease characterized by black pigmentation and gradual degeneration of the retina.

The condition is incurable and affects night and peripheral vision before gradually causing blindness in middle age.

The team  took skin samples from two patients and transformed stem cells - which can change into any cell type - into light-sensing eye cells known as photo-receptors.

They compared these with cells from healthy relatives of the patients.

Photoreceptors - which decay in retinitis pigmentosa patients - differed in their fundamental structure when compared with those from family members.

Follow-up studies in mice identified key molecules that interact with RPGR to maintain the structure of photoreceptors.

When RPGR is flawed, the structure is compromised and photoreceptors cannot function correctly, leading to sight loss.

Lead researcher said that by furthering the understanding of the RPGR gene and its effects on photoreceptor cells, they hope that these findings bring them closer to developing a possible treatment for this devastating disease.


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Friday, March 20, 2015

Could baking soda give us better vision?

Baking soda can alter how we see by modifying the visual signal generated by photo-receptors in the eyes, scientists have found.

The researchers now hope to investigate the possibility that controlling bicarbonate (baking soda) levels in the eye will slow the progress of, or may even prevent, eye diseases.

Bicarbonate in the body plays an essential role in buffering pH, aiding in digestion and neutralising lactic acid produced during physical exertion.

Much of the bicarbonate in our bodies comes from carbon dioxide, which is produced as a waste product in all cells, although some is ingested with carbonated beverages and certain types of foods.

The new study by researchers from the Massachusetts Eye and Ear/ Harvard Medical School and colleagues at Salus University, found that bicarbonate alters how we see by modifying the visual signal generated by rod and cone photo-receptors that detect light.

Within rods and cones, a small soluble molecule, cGMP, links photon absorption to the electrical activity of the photoreceptor.

In the light, cGMP is destroyed and ion channels are closed.

Positively charged sodium ions cease to enter the rod or cone and the membrane potential becomes more negative or hyperpolarised. Bicarbonate directly stimulates an enzyme called guanylate cyclase that synthesises cGMP.

"By opposing the effect of light, bicarbonate limits the size of the photon response and quickens its recovery. As a result, sensitivity to light is slightly lower but our ability to track moving objects is improved," said lead author Clint Makino, director of the Makino Laboratory at Mass Eye and Ear and an Associate Professor of Ophthalmology at Harvard Medical School.

"An intriguing implication is that vision may change with metabolic state, although further research is necessary for confirmation.

"It is now known that in some types of retinal diseases, a genetic defect causes cGMP in the rods and/or cones to rise to abnormally high, lethal levels. Once lost, rods and cones are not replaced, so an irreversible blindness is the tragic outcome," Makino said.

The study is published in the Journal of Biological Chemistry.


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Wednesday, March 06, 2013

Seven genetic risk factors found to be associated with common eye disorder

An international group of researchers has discovered seven new regions of the human genome — called loci — that are associated with increased risk of age-related macular degeneration (AMD), a leading cause of blindness. The AMD Gene Consortium, a network of international investigators representing 18 research groups, also confirmed 12 loci identified in previous studies. 


Combining data from multiple studies, this international effort provides insight into the molecular basis of AMD, which will help researchers search for causes of the disease and will inform future development of new diagnostic and treatment strategies.

AMD affects the macula, a region of the retina responsible for central vision. The retina is the layer of light-sensitive tissue in the back of the eye that houses rod and cone photoreceptor cells. Compared with the rest of the retina, the macula is especially dense with cone 
photo-receptors and is what humans rely on for tasks that require sharp vision, such as reading, driving, and recognizing faces. As AMD progresses, such tasks become more difficult and eventually impossible. Some kinds of AMD are treatable if detected early, but no cure exists. An estimated 2 million Americans have AMD.

Scientists have shown that age, diet, and smoking influence a person’s risk of developing AMD. Genetics also plays a strong role. AMD often runs in families and is more common among certain ethnicities, such as people of Asian or European descent.


Since the discovery that certain variations in the gene for complement factor H — a component of the immune system — are associated with major risk for AMD, research groups around the world have conducted genome-wide association studies to identify other loci that affect AMD risk. 

The AMD Gene Consortium combined data from 18 research groups to increase the power of prior analyses. The current analysis identified seven new loci near genes. As with the previously discovered 12 loci, these seven loci are scattered throughout the genome on many different chromosomes.

A large number of samples was needed to detect additional genetic variants that have small but significant influences on a person’s disease risk.  By cataloguing genetic variations associated with AMD, scientists are better equipped to target corresponding biological pathways and study how they might interact and change with age or other factors, such as smoking.

The 19 loci that were found to be associated with AMD implicate a variety of biological functions, including regulation of the immune system, maintenance of cellular structure, growth and permeability of blood vessels, lipid metabolism, and atherosclerosis.


As with other common diseases, such as type 2 diabetes, an individual person’s risk for getting AMD is likely determined not by one but many genes. Further comprehensive DNA analysis of the areas around the 19 loci identified by the AMD Gene Consortium could turn up undiscovered rare genetic variants with a disproportionately large effect on AMD risk. Discovery of such genes could greatly advance scientists’ understanding of AMD pathogenesis and their quest for more effective treatments. 

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