Please note this is a comparison between Version 2 by Conner Chen and Version 1 by Ivan Okhrimenko.
Alzheimer’s disease (AD) is the most common type of neurodegenerative disease in the world. Genetic evidence strongly suggests that aberrant generation, aggregation, and/or clearance of neurotoxic amyloid-β peptides (Aβ) triggers the disease. Aβ accumulates at the points of contact of neurons in ordered cords and fibrils, forming the so-called senile plaques. Aβ isoforms of different lengths are found in healthy human brains regardless of age and appear to play a role in signaling pathways in the brain and to have neuroprotective properties at low concentrations. This entry describes molecular mechanisms of amyloid-β precursor protein processing in AD.
Alzheimer’s disease
amyloid precursor protein
amyloid-β peptide
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