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Gene glitches may hold secret of a long life

Liquidus's Photo Liquidus 04 Mar 2008

From the Guardian

A series of rare genetic mutations that boost human lifespan have been discovered by a team of scientists studying centenarians and their elderly children.

The genetic glitches are thought to interfere with the normal growth of cells, halting the ageing process.

The discovery mirrors similar findings from studies on animals, which have shown that certain variations of genes linked to an insulin-like growth hormone can extend animals' lives dramatically.

Dr Nir Barzilai, director of the Institute for Ageing Research at Albert Einstein College of Medicine in New York, found a series of mutations exclusively among centenarians which affect sensitivity to "insulin growth factor 1", or IGF-1. This hormone influences the development of almost every cell in the body. It is crucial for children's growth and continues contributing to tissue generation throughout adulthood.

Barzilai's team discovered the genetic markers after scanning the genetic codes of 384 participants whose ages ranged from 95 to 110, with an average age of 100. They were compared with 312 controls, who came from families with a typical life span, none of whom had lived to 95.

Tests on cells taken from the elderly volunteers showed they were less sensitive to IGF-1, suggesting that the mutated genes were disrupting the body's ability to grow normally.

The study is published in the Proceedings of the National Academy of Sciences.


http://www.guardian....mar/04/genetics

I figured it was worth posting, it seems like relevant news.
Edited by G Snake, 04 March 2008 - 06:01 PM.
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maestro949's Photo maestro949 04 Mar 2008

Nice find.

Here's the PNAS article.

Interesting. Raises the question as to whether women live longer simply because of the same genetic causes as to why they are shorter.

In contrast, female offspring exhibited significantly higher serum IGFI and shorter stature, possibly because of variations in other genes involved in the IGF axis that may be more common than the IGF1R mutations described here.

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