Neurochemical Research

, Volume 29, Issue 3, pp 637-650

First online:

Toxicity of Amyloid β Peptide: Tales of Calcium, Mitochondria, and Oxidative Stress

  • Laura CanevariAffiliated withDivision of Neurochemistry, Institute of NeurologyMitochondrial Biology Group, Department of Physiology, UCL Email author 
  • , Andrey Y. AbramovAffiliated withDivision of Neurochemistry, Institute of Neurology
  • , Michael R. DuchenAffiliated withDivision of Neurochemistry, Institute of Neurology

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Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) peptides. Although the disease undoubtedly reflects the interaction of complex multifactorial processes, Aβ itself is toxic to neurons in vitro and the load of Aβ in vivo correlates well with the degree of cognitive impairment. There has therefore been considerable interest in the mechanism(s) of Aβ neurotoxicity. We here review the basic biology of Aβ processing and consider some of the major areas of focus of this research. It is clear that both AD and Aβ toxicity are characterized by oxidative stress, alterations in the activity of enzymes of intermediary metabolism, and mitochondrial dysfunction, especially impaired activity of cytochrome c oxidase. Studies in vitro also show alterations in cellular calcium signaling. We consider the mechanisms proposed to mediate cell injury and explore evidence to indicate which of these many changes in function are primary and which secondary.

Amyloid β peptide intracellular calcium oxidative stress mitochondria NADPH oxidase