Abstract
The heritability of human longevity is about 25% indicating scope for the identification of genes implicated in the process. Mutations in two genes, WRN and LMNA, cause premature ageing in people (progeria) which points to an effect of accumulating DNA damage in the cell as one possible mechanism of ageing. Age‐dependent accumulation of deleterious mutations in mitochondrial DNA may underly some ageing processes especially in the nervous system. Longevity in mice is also influenced by the rate of cell proliferation and apoptosis leading to correlations between longevity and both body size and length of chromosome telomeres. Across all organisms age is accompanied by reduced expression of genes involved in oxidative metabolism and interest in the connections between diet and longevity has been stimulated by the recent observation that the drug rapamycin extends lifespan in mice. This drug interferes with cell nutrition by inhibiting the TOR signalling pathway.
Original language | English |
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Title of host publication | Principles and Practice of Geriatric Psychiatry |
Subtitle of host publication | Third Edition |
Editors | Mohammed T. Abou‐Saleh , Cornelius Katona, Anand Kumar |
Publisher | John Wiley & Sons Inc. |
Pages | 51-54 |
Number of pages | 4 |
ISBN (Print) | 9780470747230 |
DOIs | |
Publication status | Published - 2 Dec 2010 |
Keywords
- body size
- diet
- DNA repair
- mitochondria
- progeria
- rapamycin
- telomere
- TOR signalling