期刊
AGEING RESEARCH REVIEWS
卷 9, 期 4, 页码 447-456出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2010.05.003
关键词
Mitochondria; Calcium; Alzheimer's disease; Voltage dependent anion channel; Mitochondrial membrane potential
资金
- GRF [755206M, 761609M]
- NSFC/RGC [N_HKU 707107M]
- HKU Seed Funding for Basic Science Research [200911159082]
- HKU Alzheimer's Disease Research Network
- Strategic Theme Research for Drug Discovery
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. (C) 2010 Elsevier B.V. All rights reserved.
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