Tags: Alzheimer's/Dementia | Alzheimers | disease | macular | degeneration | blindness

Alzheimer's Proteins May Contribute to Blindness

Alzheimer's Proteins May Contribute to Blindness

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By    |   Tuesday, 22 November 2016 02:40 PM

The accumulation of proteins linked to Alzheimer’s disease could be one of the causes of age-related macular degeneration, a leading cause of blindness in older people.

Age-related macular degeneration (AMD) is the leading cause of vision loss among people age 50 and older.

The disease causes damage to the macula, a small spot near the center of the retina and the part of the eye needed for sharp, central vision, which lets us see objects that are straight ahead.

Now researchers have discovered that a group of proteins, which are linked to Alzheimer's disease, are able to accumulate in the retina and damage it.

There are two different types of AMD -- 'wet' and 'dry'. In wet AMD, the growth of leaky blood vessels, which damage the retina, can be stopped.. However, this does not work for everyone, and is a way to manage rather than cure wet AMD. By contrast, dry AMD has no approved treatment as yet.

The study, which was done by researchers in the UK used both cell cultures and mouse models, analyzing how quickly amyloid beta proteins, which are thought to be a likely cause of Alzheimer's disease, entered the retina and how they damaged it.

The team found that the amyloid beta proteins entered the cells of the retina within 24 hours of exposure and then began to break the cell's scaffold structure.

The next step will be to evaluate how the amyloid beta proteins get into retinal cells and study more closely how damage occurs, with a view of establishing preventative measures or treatment options, the researchers say of the study, which appears in Experimental Eye Research.


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Age-related macular degeneration is a leading cause of blindness and now a new study finds that proteins linked to Alzheimer's disease may contribute to it.
Alzheimers, disease, macular, degeneration, blindness
Tuesday, 22 November 2016 02:40 PM
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