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Lookup NU author(s): Kim Krishnan, Heidi De Gruyter, Dr Evelyn Jaros, Emeritus Professor Doug Turnbull
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Alzheimer's disease (AD) is the most common form of dementia, increasing in prevalence with age. Most patients who develop AD have an unknown cause, but characteristic neuropathological features include the deposition of extracellular amyloid beta and of intraneuronal hyperphosphorylated tau protein. Researchers have previously implicated mitochondrial dysfunction in AD. We previously showed an increase in neurons displaying a mitochondrial biochemical defect-cytochrome-c oxidase (COX) deficiency-in the hippocampus in patients with sporadic AD compared with age-matched controls. COX deficiency is well described as a marker of mitochondrial (mt) DNA dysfunction. This present study analyzed the mtDNA in single neurons from both COX normal and COX-deficient cells. Analysis of the mtDNA revealed that COX deficiency is caused by high levels of mtDNA deletions which accumulate with age. Future research is needed to clarify the role mtDNA deletions have in normal aging and investigate the relationship between mtDNA deletions and the pathogenesis of sporadic AD. (C) 2012 Elsevier Inc. All rights reserved.
Author(s): Krishnan KJ, Ratnaike TE, De Gruyter HLM, Jaros E, Turnbull DM
Publication type: Article
Publication status: Published
Journal: Neurobiology of Aging
Year: 2012
Volume: 33
Issue: 9
Pages: 2210-2214
Print publication date: 01/09/2012
ISSN (print): 0197-4580
ISSN (electronic): 1558-1497
Publisher: Elsevier Inc.
URL: http://dx.doi.org/10.1016/j.neurobiolaging.2011.08.009
DOI: 10.1016/j.neurobiolaging.2011.08.009
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