One change that occurs in the retina of people with AMD as the disease progresses is an increase in the number and size of fatty deposits called drusen.
In their study paper, the researchers explain that the causes of AMD are understood to be complex, with both genetic as well as environmental risks factors, and share similarities with Alzheimer’s disease.
They note how recent studies have shed a lot of light on the genetic causes of AMD – although this is not matched by insights into the molecular mechanisms involved.
However, they also note that other studies have found aged and AMD retinas also show accumulation of the types of beta-amyloid proteins that are found in toxic plaques in the brains of people with Alzheimer’s disease, and “for which there appears to be no clear genetic basis.”
For their study, Dr. Arjuna Ratnayaka, a lecturer in vision sciences at Southampton, and colleagues used cell cultures and mouse models of AMD to investigatemechanisms of Alzheimer’s beta-amyloid accumulation inside retinal cells.
They were particularly interested in the speed with which the proteins find their way inside the retinal cells.
The researchers found the retinal cells internalized the amyloid proteins within 24 hours of being exposed to them.
They also discovered that the amyloid proteins are retained inside the retinal cells, where they gradually impair a molecular mechanism reliant on the protein encoded by the MAP-2 gene. Among other things, MAP-2 mechanisms help to maintain important structures inside cells called microtubules.
Dr. Ratnayaka says they were surprised at the speed with which the amyloid proteins entered the cells, and he suggests the finding may help explain how a healthy retina can switch to a diseased, AMD retina.
The team is now planning to evaluate how the beta-amyloid proteins actually enter the retinal cells and set about causing internal damage. The hope is the continuing work will lead to measures to prevent or treat AMD.
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