The amyloid hypothesis for Alzheimer's disease: a critical reappraisal

J Neurochem. 2009 Aug;110(4):1129-34. doi: 10.1111/j.1471-4159.2009.06181.x. Epub 2009 May 18.

Abstract

The amyloid hypothesis has been the basis for most work on the pathogenesis of Alzheimer's disease. Recent clinical trials based on this hypothesis have been inconclusive. In this article I review the current status of the hypothesis and suggest that a major scientific need is to understand the normal function of amyloid-beta precursor protein (APP) and think how this may relate to the cell death in the disease process.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / etiology*
  • Alzheimer Disease / metabolism
  • Alzheimer Vaccines / adverse effects
  • Amyloid beta-Peptides / antagonists & inhibitors
  • Amyloid beta-Peptides / immunology
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / metabolism*
  • Brain / drug effects*
  • Brain / metabolism
  • Brain / physiopathology*
  • Cerebral Arteries / drug effects
  • Cerebral Arteries / metabolism
  • Cerebral Arteries / physiopathology
  • Clinical Trials as Topic / methods
  • Clinical Trials as Topic / standards
  • Disease Progression
  • Humans
  • Nerve Degeneration / drug therapy
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / physiopathology

Substances

  • Alzheimer Vaccines
  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor