Mitochondria and the pathogenesis of ALS

doi:10.1093/brain/123.7.1291

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Brain, Vol. 123, No. 7, 1291-1292, July 2000
© 2000 Oxford University Press

Editorial

Mitochondria and the pathogenesis of ALS

M. Flint Beal

Department of Neurology, Weill Medical College, and Department of Neurology, New York Presbyterian Hospital, Cornell University, New York, USA

Evidence implicating mitochondria as playing a crucial rolein both necrotic and apoptotic cell death is rapidly accumulating.Mitochondria are essential in controlling specific apoptosispathways (Green and Reed, 1998). Mitochondrial calcium uptakeis required for glutamate excitotoxicity and there is a correlationbetween increases in mitochondrial calcium and increases infree radical generation, which are linked with cell death (Stoutet al., 1998). The mitochondrial permeability transition poremay be crucial in both necrotic and apoptotic cell death. Activationof the permeability transition pore increases the mitochondrialmembrane permeability to solids . . . [Full Text of this Article]

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