Cottrell D A, Turnbull D M
Department of Neurology, The Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK.
Curr Opin Clin Nutr Metab Care. 2000 Nov;3(6):473-8. doi: 10.1097/00075197-200011000-00009.
Mitochondria have long been proposed as a perpetrator of aging. We review here the accumulating evidence for chronological alterations in the mitochondrion and discuss how these changes may cause cellular dysfunction and death. We conclude that although the evidence for aging changes in the level of oxidative stress, DNA mutations and biochemical deficiencies in mitochondria are convincing, there is little experimental evidence to link these changes directly with the cellular pathology of aging. Promising avenues for addressing this problem include the investigation of established mitochondrial DNA disorders and the development of animal models with mitochondrial defects.
