Alzheimer’s disease is characterized by the accumulation of aggregated Aβ peptides in senile plaques and vascular deposits. Aβ peptides are derived from amyloid precursor protein (APP) through sequential proteolytic cleavage of APP by β- and γ-secretases generating diverse Aβ species. Aβ can aggregate to form soluble oligomeric species and insoluble fibrillar or amorphous assemblies. Some forms of the aggregated peptides are toxic to neurons.
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