Linked Life Data

12414225

Source:http://linkedlifedata.com/resource/pubmed/id/12414225

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9342
pubmed:dateCreated
2002-11-4
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
360
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1323-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Accumulation of mitochondrial DNA mutations in ageing, cancer, and mitochondrial disease: is there a common mechanism?
pubmed:affiliation
Departments of Neurology, University of Newcastle upon Tyne, NE2 4HH, Newcastle upon Tyne, UK. p.f.chinnery@ncl.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't