Modulation of mitochondrial calcium as a pharmacological target for Alzheimer's disease

Clara Hiu Ling Hung, Yuen Shan Ho, Raymond Chuen Chung Chang

Research output: Journal article publicationReview articleAcademic researchpeer-review

42 Citations (Scopus)


Perturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca2+) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca2+uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca2+is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria. This review critically discusses the potential of manipulating mitochondrial Ca2+concentrations as a novel therapeutic opportunity for treating AD. This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca2+transport pathways. It is reasoned that these mitochondrial Ca2+modulators are most effective in combination with agents that increase the Ca2+buffering capacity of mitochondria. Modulation of mitochondrial Ca2+handling is a potential pharmacological target for future development of AD treatments.
Original languageEnglish
Pages (from-to)447-456
Number of pages10
JournalAgeing Research Reviews
Issue number4
Publication statusPublished - 1 Oct 2010
Externally publishedYes


  • Alzheimer's disease
  • Calcium
  • Mitochondria
  • Mitochondrial membrane potential
  • Voltage dependent anion channel

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Ageing
  • Molecular Biology
  • Neurology


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