Journal
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Volume 464, Issue 1, Pages 111-121Publisher
SPRINGER
DOI: 10.1007/s00424-012-1112-0
Keywords
Mitochondria; Intracellular calcium; Neurodegenerative disease; Glutamate excitotoxicity
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Funding
- Wellcome Trust
- Medical Research Council
- MRC [MC_G1000735] Funding Source: UKRI
- Medical Research Council [MC_G1000735] Funding Source: researchfish
- Parkinson's UK [G-1101] Funding Source: researchfish
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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.
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