Premium
Molecular gerontology
Author(s) -
Kirkwood T. B. L.
Publication year - 2002
Publication title -
journal of inherited metabolic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 102
eISSN - 1573-2665
pISSN - 0141-8955
DOI - 10.1023/a:1015625811569
Subject(s) - longevity , ageing , oxidative damage , dna damage , biology , gerontology , psychological intervention , cellular metabolism , cellular aging , dna repair , bioinformatics , medicine , metabolism , genetics , gene , oxidative stress , dna , biochemistry , psychiatry , telomere
Evolutionary theory and empirical evidence from many lines of research suggest that ageing is a process of gradual accumulation of damage in cells and tissues of the body, leading eventually to frailty and increased risk from a spectrum of age‐associated diseases. There are multiple kinds of damage that affect cells, ranging from mutations in DNA to oxidative attack on proteins by chemical by‐products of normal cellular metabolism. In some ways the surprising thing is not that we age, but that we live as long as we do. The key to understanding longevity lies in the network of cell maintenance systems that cooperate to slow the accumulation of damage. Research has shown that long‐lived species carry out cellular maintenance better than short‐lived species, suggesting that enhancement of the body's natural maintenance systems may postpone aspects of ageing. Recognition that ageing results from accumulation of damage also points to a role for lifestyle interventions (e.g. nutrition and exercise) to help prevent damage or promote repair.