The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Science. 2002 Jul 19;297(5580):353-6. doi: 10.1126/science.1072994.

Abstract

It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / etiology*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology
  • Amino Acid Sequence
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / chemistry
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Anticholesteremic Agents / therapeutic use
  • Brain / metabolism*
  • Brain / pathology
  • Clinical Trials as Topic
  • Humans
  • Molecular Sequence Data
  • Nerve Degeneration
  • Neurofibrillary Tangles / metabolism
  • Neurofibrillary Tangles / pathology
  • Neurons / pathology
  • Plaque, Amyloid / pathology
  • Protease Inhibitors / therapeutic use
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Anti-Inflammatory Agents
  • Anticholesteremic Agents
  • Protease Inhibitors
  • tau Proteins