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Review
. 1999 Jan-Feb;20(1):65-9.
doi: 10.1016/s0197-4580(99)00014-7.

Hypothesis: amyloid beta-peptides truncated at the N-terminus contribute to the pathogenesis of Alzheimer's disease

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Review

Hypothesis: amyloid beta-peptides truncated at the N-terminus contribute to the pathogenesis of Alzheimer's disease

A J Larner. Neurobiol Aging. 1999 Jan-Feb.

Abstract

Fragments of amyloid beta-peptide truncated at the N-terminus are present in AD brain early in the course of Alzheimer's disease. It is proposed that these species contribute to the pathogenesis of AD, possibly through destabilization of elements of the neuronal cytoskeleton by small fibrillar deposits.

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