Mitochondria, calcium-dependent neuronal death and neurodegenerative disease

作者：Michael R. Duchen · 发表于：Pflügers Archiv - European Journal of Physiology · 年份：2012 · DOI：10.1007/s00424-012-1112-0 · 被引用次数：187 · 研究领域：Parkinson's Disease Mechanisms and Treatments、Mitochondrial Function and Pathology、Genetic Neurodegenerative Diseases

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.