Proteins that control visual system development in the young brain appear to affect susceptibility to Alzheimer’s disease in the aging brain, according to research results funded in part by the National Eye Institute, National Institute on Aging, and the National Institute of Neurological Disorders and Stroke.
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During the course of Alzheimer’s disease, large plaques of beta-amyloid and other proteins accumulate in the brain. Even in the absence of plaques, beta-amyloid has been shown to damage brain cells and synapses.
Carla Shatz, PhD, the study’s lead investigator, discovered that mice without a gene for PirB, a protein on the surface of nerve cells in the mouse brain, have an increase in ocular dominance plasticity. Ocular dominance plasticity is the competition of the eyes to connect within a limited territory of the brain.
Researchers found that PirB binds tightly to beta-amyloid that are believed to ultimately grow into plaques. Without PirB, the synapses in the mouse brain were resistant to the effects of beta-amyloid.
Humans have a closely related protein called LilrB2. Researchers found supporting evidence that LIlrB2 may trigger the same harmful reactions that PirB can trigger in the mouse brain by binding to beta-amyloid.
Dr. Shatz and colleagues were able to conclude that LilrB2 in humans and PirB in mice can physically partner with beta-amyloid. When PirB was depleted in the mouse’s brain, it prevented the harmful chain reaction and reduced memory loss. Currently, only two other beta-amyloid receptors (PrP-C and EphB2) have been found and are being tracked as drug targets.
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