A principal neuropathological hallmark of Alzheimer's disease is deposition of beta-amyloid, composed primarily of a 4 kD peptide, A beta. This peptide is derived from larger amyloid precursor proteins. The mechanisms that are responsible for A beta 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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