Has the Amyloid Cascade Hypothesis for Alzheimers Disease been Proved?

John      Hardy

doi:10.2174/156720506775697098

Abstract

After much initial debate for and against the role of amyloid in Alzheimers disease (AD), mutations on the amyloid precursor protein (APP) and processing pathways that increase levels of the amyloid b peptide of 42 residues (Aβ42) have established that faulty function or processing of these proteins are responsible for AD pathogenesis. Given the neurotoxicity of aggregates of Ab42, the central role of this peptide in AD pathogenesis is self evident. In this article, I summarize the major pieces of evidence adduced to support the amyloid cascade hypothesis and point out their limitations

Keywords: APP mutations, neurodegenerative disease, oxidative stress, apolipoprotein, presenilin

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