Mutant genes ‘key to long life’

There is a clear link between living to 100 and inheriting a hyperactive version of an enzyme that prevents cells from ageing, researchers say.

Scientists from the Albert Einstein College of Medicine in the US say centenarian Ashkenazi Jews have this mutant gene.

They found that 86 very old people and their children had higher levels of telomerase which protects the DNA. Telomeres are relatively short sections of specialized DNA that sit at the ends of all our chromosomes. They have been compared to the plastic tips at the ends of shoelaces that prevent the laces from unravelling. Each time a cell divides, its telomeres shorten and the cell becomes more susceptible to dying. Telomerase can repair the telomeres, preventing them from shrinking.

The team at Einstein found that the centenarians and their offspring had higher levels of telomerase and significantly longer telomeres than the unrelated people in the control group and that the trait was strongly heritable.

To read the full article on the BBC health news pages, click here

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6 Responses to Mutant genes ‘key to long life’

  1. theagingfanboy says:

    So old people have lived longer than people who died before they did. Who’d have thunk it? Seriously, the fact that old age runs in families has been commented on before, but now that everyone (here at least) has a good chance of living beyond retirement it may turn out that teleomeres aren’t the easy explanation that was once thought.

  2. methusela says:

    I’m afraid agingfanboy is a bit confused about potential and actual lifespan. The reason most of us in industrialised countries now reach three score years and ten (at least) is because we are far less likely to die of childhood illnesses and infections, for a combination of reasons (innoculation, antibiotics, better public hygiene, etc). However, assuming we reach old age, how much longer we live is rather more down to genes. This has been known for a long while – if you compare people living now versus those living in any period in the historical past, the difference in life expectancy at birth is vast (a matter of decades in many cases). However, the difference in life expectancy between people already in their eighties and older is tiny (often a matter of a few months). In other words, there’s only so much that environment can do to increase life expectancy and in the oldest old, it appears to have little effect.

    That does not mean that telomeres are the answer to everything related to longevity. Longer telomeres seem to play a role, but it would be simplistic to assume that this is the sole answer. Apart from anything else, telomerase is implicated in causing various cancers (essentially, by creating ‘zombie cells’ by reviving ageing cells that should have died).

  3. methusela says:

    I’m afraid agingfanboy is a bit confused about potential and actual lifespan. The reason most of us in industrialised countries now reach three score years and ten (at least) is because we are far less likely to die of childhood illnesses and infections, for a combination of reasons (innoculation, antibiotics, better public hygiene, etc). However, assuming we reach old age, how much longer we live is rather more down to genes. This has been known for a long while – if you compare people living now versus those living in any period in the historical past, the difference in life expectancy at birth is vast (a matter of decades in many cases). However, the difference in life expectancy between people already in their eighties and older is tiny (often a matter of a few months). In other words, there’s only so much that environment can do to increase life expectancy and in the oldest old, it appears to have little effect.

    That does not mean that telomeres are the answer to everything related to longevity. Longer telomeres seem to play a role, but it would be simplistic to assume that this is the sole answer. Apart from anything else, telomerase is implicated in causing various cancers (essentially, by creating ‘zombie cells’ by reviving ageing cells that should have died).

  4. theagingfanboy says:

    Listen carefully, for I shall post this only once……. It seems to me that what you say agrees with my post entirely. When I said: “everyone (here at least)” I meant because there is better public health here and we get a chance to die of old age. When I said: “it may turn out that teleomeres aren’t the easy explanation that was once thought” I meant that it would be simplistic to assume that this is the sole answer. My first sentence referred to the fact that the subjects had been chosen on the basis of their advanced age. For all we know thee may be whole groups of people with long telomeres who die before retirement age.

  5. methusela says:

    There may indeed be folks with long telomeres who die young. However, in animals with shorter life spans (where we can measure their llifespans within the limits of a grant) there does seem to be evidence that overall, long telomeres = longer lifespan. Of course there will always be the exceptions.

  6. theagingfanboy says:

    There’s no doubt that’s true. It could even be that cloned animals will be born with “pre-aged” cells, as the adult cells they’re cloned from have shorter telomeres to start off with. As for “natural lifespans”, they’re not too reliable, as virtually nothing in the natural world ever lives long enough to die of old age, so presumably there’s no selection pressure on telomeres in ordinary body cells.

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