Mitochondria, Calcium and Cell Death: A Deadly Triad in Neurodegeneration

Biochim Biophys Acta. 2009 May;1787(5):335-44. doi: 10.1016/j.bbabio.2009.02.021. Epub 2009 Mar 4.

Abstract

Mitochondrial Ca(2+) accumulation is a tightly controlled process, in turn regulating functions as diverse as aerobic metabolism and induction of cell death. The link between Ca(2+) (dys)regulation, mitochondria and cellular derangement is particularly evident in neurodegenerative disorders, in which genetic models and environmental factors allowed to identify common traits in the pathogenic routes. We will here summarize: i) the current view of mechanisms and functions of mitochondrial Ca(2+) homeostasis, ii) the basic principles of organelle Ca(2+) transport, iii) the role of Ca(2+) in neuronal cell death, and iv) the new information on the pathogenesis of Alzheimer's, Huntington's and Parkinson's diseases, highlighting the role of Ca(2+) and mitochondria.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology
  • Calcium / physiology*
  • Cell Death / physiology*
  • Cytosol / metabolism
  • Humans
  • Huntingtin Protein
  • Huntington Disease / pathology
  • Huntington Disease / physiopathology
  • Mitochondria / physiology*
  • Mitochondrial Membranes / physiology
  • Mutation
  • Nerve Degeneration / genetics
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology*
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / physiology
  • Nuclear Proteins / genetics
  • Parkinson Disease / pathology
  • Parkinson Disease / physiopathology
  • Presenilins / physiology
  • Signal Transduction
  • Ubiquitin-Protein Ligases / genetics

Substances

  • HTT protein, human
  • Huntingtin Protein
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Presenilins
  • Ubiquitin-Protein Ligases
  • parkin protein
  • Calcium