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Gene mutation might hold key to longer life
Ageing has become a subject of considerable interest in many developed countries with an ageing population, both in terms of health and social care policy development, and scientific research. The underlying genetic mechanisms and biological pathways involved in the ageing process have been an area of biomedical research for some years; for useful review see Martin GM, Bergman A, Barzilai N. PLoS Genet. 2007 Jul;3(7):e125 and published and a Nature supplement on ageing published last year. Ultimately, the aim of research into ageing is to develop interventions and strategies that might boost normal life span.
A new publication has reported rare genetic mutations that appear to be associated with a longer life span; research based around a group of nearly 400 Ashkenazi Jews between the ages of 95 and 108 has led to the identification of two mutations that affect how cells respond to a particular growth factor, termed insulin-like growth factor 1, or IGF1 [Suh Y et al. Proc Natl Acad Sci U S A. 2008 Mar 4;105(9):3438-42]; see also press reports from 4th March in the Guardian and the Medical News Today.
IGF1 is crucial for normal growth in children, and it influences tissue generation in adults.It is already known that defects in the activity of this hormone can almost double the normal lifespan in yeasts, mice, nematodes and flies. Until now, however, it has not been possible to identify a similar link in humans because of the lack of suitable control groups. To overcome this, the researchers investigated both the centenarians and their children (aged 49-88 years) alongside a control group provided by Ashkenazi Jews of similar ages without a family history of unusual longevity.
The study shows that the female (but not male) offspring of the centenarians have higher concentrations of IGF1 in their bloodstream than do controls, leading the authors to suggest that there is a defect in this pathway. Indeed, genetic analysis of the receptor through which IGF-I mediates its effects identified two mutations that were more common in long-lived families than in controls and that reduce the sensitivity of cells to IGF1. However, the reason for the increased in IGF1 in females but not males remains unclear.
Although more common in long-lived families, these mutations are still rare, leaving open the question of what other factors may be involved. No doubt ageing, in common with complex diseases, involves multiple different genetic and environmental factors (for example, see previous news). Further studies comparing the genetic make-up of long-lived individuals and families with normal age-span may reveal new insights into the process.
Keywords: Genetic Databases