Amyloid beta-peptide and oxidative cellular injury in Alzheimer's disease

Mol Neurobiol. 1996 Jun;12(3):211-24. doi: 10.1007/BF02755589.


Alzheimer's disease is a progressive neurodegenerative disorder that affects primarily learning and memory functions. There is significant neuronal loss and impairment of metabolic functioning in the temporal lobe, an area believed to be crucial for learning and memory tasks. Aggregated deposits of amyloid beta-peptide may have a causative role in the development and progression of AD. We review the cellular actions of A beta and how they can contribute to the cytotoxicity observed in AD. A beta causes plasma membrane lipid peroxidation, impairment of ion-motive ATPases, glutamate uptake, uncoupling of a G-protein linked receptor, and generation of reactive oxygen species. These effects contribute to the loss of intracellular calcium homeostasis reported in cultured neurons. Many cell types other than neurons show alterations in the Alzheimer's brain. The effects of A beta on these cell types is also reviewed.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / physiology*
  • Animals
  • Brain / pathology
  • Brain / physiopathology*
  • Cerebrovascular Circulation
  • Free Radicals
  • Humans
  • Lymphocytes / physiology
  • Models, Neurological
  • Neuroglia / pathology
  • Neuroglia / physiology
  • Neurotoxins
  • Oxidative Stress*
  • Reactive Oxygen Species
  • Signal Transduction


  • Amyloid beta-Peptides
  • Free Radicals
  • Neurotoxins
  • Reactive Oxygen Species