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Pflugers Arch. 2012 Jul;464(1):111-21. doi: 10.1007/s00424-012-1112-0. Epub 2012 May 22.

Mitochondria, calcium-dependent neuronal death and neurodegenerative disease.

Author information

1
Department of Cell and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK. m.duchen@ucl.ac.uk

Abstract

Understanding the mechanisms of neuronal dysfunction and death represents a major frontier in contemporary medicine, involving the acute cell death in stroke, and the attrition of the major neurodegenerative diseases, including Parkinson's, Alzheimer's, Huntington's and Motoneuron diseases. A growing body of evidence implicates mitochondrial dysfunction as a key step in the pathogenesis of all these diseases, with the promise that mitochondrial processes represent valuable potential therapeutic targets. Each disease is characterised by the loss of a specific vulnerable population of cells--dopaminergic neurons in Parkinson's disease, spinal motoneurons in Motoneuron disease, for example. We discuss the possible roles of cell type-specific calcium signalling mechanisms in defining the pathological phenotype of each of these major diseases and review central mechanisms of calcium-dependent mitochondrial-mediated cell death.

PMID:
22615071
PMCID:
PMC3387496
DOI:
10.1007/s00424-012-1112-0
[Indexed for MEDLINE]
Free PMC Article

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