Amyloid-β

Amyloid-β (Aβ) denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer's disease as the main component of theamyloid plaques found in the brains of Alzheimer patients. The peptides result from the amyloid precursor protein (APP), which is being cut by certain enzymes to yield Aβ. Amyloid-β molecules can aggregate to form flexible soluble oligomers which may exist in several forms. Amyloid-β peptide is due to overproduction of Aβ and/or the failure of clearance mechanisms. Amyloid-β self-aggregates into oligomers, which can be of various sizes, and forms diffuse and neuritic plaques in the parenchyma and blood vessels. Amyloid-β oligomers and plaques are potent synaptotoxins, block proteasome function, inhibit mitochondrial activity, alter intracellular Ca²⁺levels and stimulate inflammatory processes. Loss of the normal physiological functions of Aβ is also thought to contribute to neuronal dysfunction.