Guest guest Posted October 25, 2002 Report Share Posted October 25, 2002 Hi All, I can send the whole paper of the attached abstract if requested. but wonder whether the figure can work so this is an experiment first. Cheers, Al. Alan Pater, Ph.D.; Faculty of Medicine; Memorial University; St. 's, NL A1B 3V6 Canada; Tel. No.: (709) 777-6488; Fax No.: (709) 777-7010; email: apater@... Lancet 2002; 360: 1323-25 Hypothesis Accumulation of mitochondrial DNA mutations in ageing, cancer, and mitochondrial disease: is there a common mechanism? F Chinnery, C s, Joanna Elson, s M Turnbull . In man, cells accumulate somatic mutations of mitochondrial DNA (mtDNA) as part of normal ageing. Although the overall concentration of mutant mtDNA is low in tissue as a whole, very high numbers of various mtDNA mutations develop in individual cells within the same person, which causes age-associated mitochondrial dysfunction. Some tumours contain high numbers of mtDNA mutations that are not present in healthy tissues from the same individual. The proportion of mutant mtDNA also rises in patients with progressive neurological disease due to inherited mtDNA mutations. This increase parallels the relentless clinical progression seen in these disorders. Mathematical models suggest that the same basic cellular mechanisms are responsible for the amplification of mutant mtDNA in ageing, in tumours, and in mtDNA disease. The accumulation of cells that contain high levels of mutant mtDNA may be an inevitable result of the normal mechanisms that maintain cellular concentrations of mtDNA. Quote Link to comment Share on other sites More sharing options...
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