Фонд Авангарда
Alzheimer's Disease
Alzheimer's Disease (AD) is a progressive neurodegenerative disease that affects roughly 55 million worldwide. It's the most common cause of dementia and presents with memory issues, behavioral changes, and gradual decline in cognitive function. AD is marked by abnormal accumulation of beta-amyloid plaques and tau tangles, which disrupt normal neuronal communication and ultimately lead to neuronal damage.
Beta-Amyloid Plaques
Amyloid precursor protein (APP) is a type-I membrane protein, known for its role in cell proliferation and differentiation as well as neuronal repair. In Alzheimer’s (AD), Beta-amyloid protein is formed from the proteolysis of APP by beta-secretase (extracellular) and then by gamma-secretase (in the membrane). The buildup of beta-amyloid protein forms oligomeric beta-amyloid and plaques, a marker of Alzheimer’s disease. Beta-amyloid protein toxicity leads to neuronal death, impaired cognitive functions (including behavioral changes), and synaptic dysfunction.
Tau Tangles
In AD, tau protein (which normally binds to microtubules) detach from microtubules and sticks together, forming tangles within neurons. This occurs following hyperphosphorylation of the tau protein. Tau tangles can inhibit synaptic communication between neurons resulting in cognitive decline.