Abstract

Alzheimer's disease (AD) is a neurodegenerative disease characterized by extracellular amyloid-β (Aβ) plaques that form toxic aggregates and lesions. The underlying cause of AD is unknown, but studies have shown that several familial AD (FAD) mutations of Aβ lead to early onset and a more severe form of the disease. The “Iowa” D23N, “Arctic” E22G, “Italian” E22K, and “Dutch” E22Q variants of Aβ contain charge-altering mutations that have been shown to accelerate the rate of aggregation relative to the wild-type (WT) peptide.

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