A principal neuropathological hallmark of Alzheimer's disease is deposition of β-amyloid, composed primarily of a 4 kD peptide, Aβ. This peptide is derived from larger amyloid precursor proteins. The mechanisms that are responsible for Aβ formation in vivo are unknown. Recently, transgenic strategies have been employed to test several hypothetical mechanisms in order to reproduce Alzheimer's disease-specific pathology in rodents.
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