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a Mitochondrial Research Group, Neurology, University of Newcastle upon Tyne, Medical School, Framlington Place, NE2 4HH Newcastle upon Tyne, United Kingdom
Key Words: mitochondria • aging • mtDNA mutations • reactive oxygen species
Address for correspondence: Prof. D. M. Turnbull, Mitochondrial Research Group, School of Neurology, Neurobiology and Psychiatry, The Medical School, Newcastle University, Framlington Place, NE2 4HH, Newcastle upon Tyne, UK. Voice: +(44)01912228334; fax: +(44)0192228553. d.m.turnbull{at}ncl.ac.uk
Mitochondria have been hypothesized to play a role in both aging and neurodegenerative diseases, such as Parkinson's disease (PD) and Alzheimer's disease. Many studies have shown the accumulation of mitochondrial DNA (mtDNA) mutations in post-mitotic tissues and more recent data have shown this also to be a feature of aging mitotic tissues. Much of this data has been correlative, until recently with the development of polymerase gamma deficient mice which accumulate high levels of mtDNA mutations and show a premature aging phenotype, that a more causative role has been proposed. This article focuses on recent developments in aging research into the role that mtDNA mutations play in the aging process.
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