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

Abstract:

:Perturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca(2+)) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca(2+) uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca(2+) 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 Ca(2+) 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 Ca(2+) transport pathways. It is reasoned that these mitochondrial Ca(2+) modulators are most effective in combination with agents that increase the Ca(2+) buffering capacity of mitochondria. Modulation of mitochondrial Ca(2+) handling is a potential pharmacological target for future development of AD treatments.

journal_name

Ageing Res Rev

journal_title

Ageing research reviews

authors

Hung CH,Ho YS,Chang RC

doi

10.1016/j.arr.2010.05.003

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

447-56

issue

4

eissn

1568-1637

issn

1872-9649

pii

S1568-1637(10)00046-2

journal_volume

9

pub_type

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