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New theory of aging points the finger at misrepairs

It’s not cellular and molecular damage that causes aging but the accumulation of misrepairs

The question of how and why we age is of more than passing interest for most people. And yet we know very little about it. Today, Thomas Michelitsch at the Université Pierre et Marie Curie in Paris and a couple of amis, propose a radical new idea to explain how and why our bodies age.

Two main theories of aging have dominated thinking in this area. On the one hand is the argument that aging is regulated by our genes, an idea that is backed up by various studies showing that some genes can dramatically increase lifespan (if you happen to be a nematode worm, for example).

On the other is the notion that aging is the result of the accumulation of various faults on the cellular and molecular level, caused by environmental factors such as free radicals and molecular cross-linking.

In reality, most researchers think that both mechanisms play an important role.

The new idea from Michelitsch and co relates to this second mechanism. They contend that the accumulation of faults on the cellular and molecular level are certainly involved in aging but are not the mechanism of aging. These faults trigger the body’s repair mechanisms, which fix everything up, most of the time.

But sometimes these repair mechanisms go wrong, leaving small regions of misrepair. The new idea is that aging is the result of the accumulation of these misrepairs over time.

This leads to a key prediction about aging. The team says: “Our theory suggests that for extending lifespan all efforts need to focus on the reduction of misrepair.”

So what should you do if you want to live longer? Avoid damage as far as possible, say Michelitsch and pals, emphasising that “it is especially important to prevent chronic inflammation, which is an important source of misrepair.”

Ref: arxiv.org/abs/0904.0575: Aging as a Consequence of Misrepair– a Novel Theory of Aging

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