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Repairing Mitochondria to Help Stop Aging

posted on July 2, 2007

66 year old Dr. Stephen Coles, co-founder and president of Gerontological Research Group has apparently discovered the Fountain of Youth.

Last Saturday, Dr. Coles married a beautiful 26 year. Congratulations to Steve and Natalie. I will make sure we all get invited to their Golden Anniversary celebration.


Mitochondria are the power plants of your cells, evolved from symbiotic bacteria and bearing their own DNA. They transform food into the molecule ATP, used by cellular processes for energy, but mitochondria and their DNA become damaged and mitochondrial function declines with advancing age. As more is discovered and the tools of modern biotechnology improve, the repair of damaged mitochondria as a strategy to help halt or reverse aging looks ever more plausible with each passing year.

In recent months, some researchers have suggested that ongoing decline in mitochondrial function is the cause of two other biochemical processes linked with aging and specific age-related conditions. Firstly, that shortened telomeres rest on mitochondrial damage:

Secondly, that declining ability to repair DNA damage also might have the same root cause:

Both DNA damage and telomere shortening are widely considered to contribute to age-related degeneration – as for so much of aging science, definitive mechanisms and absolute answers are still up for debate, however. Neither of the “mitochondria did it” proposals above has yet had time to be widely debated and further investigated, but this is not to mention the direct role of mitochondrial DNA damage in causing age-related degeneration in the well-supported mitochondrial free radical theory of aging:

A successful strategy to defeat aging – defeat, not just slow – must look at the biochemical changes that occur with aging, treat those changes as damage, and repair them. We shouldn’t follow the cues of past decades and merely aim to patch over the symptoms of aging, or merely aim to slow aging, as that is an expensive way of failing. The more researchers understand our biochemistry, the better they can identify which age-related changes are truly fundamental – to strike at the root, with less effort and more rapid results. But as for the bridge builders of past millennia, we don’t necessarily need complete understanding to start now and produce good work:

It will be fortunate if mitochondrial damage turns out to be a more important root cause of aging than previously thought, as scientists have already created technology demonstrations for a variety of ways to repair that damage… or make it irrelevant. In the latter category are efforts to move fragile mitochondrial DNA – genes – into the well-protected cellular nucleus. These efforts received a boost with recently published work:

“The job of a gene is, in essence, to act as the instruction set for the production of proteins, the components of cellular machinery. A core problem in moving the factory from the mitochondria to the nucleus is that these proteins would then have to struggle their way back to the mitochondria where they are needed; this has been a challenge for a variety of reasons.

“These researchers have demonstrated a way to overcome that challenge for at least a subset of mitochondrial genes – via what might be viewed as a rather clever hack to the programming of the cell – and thus can repair dysfunctional mitochondria which results from damage to those genes and a local absence of vital proteins.”

Pay attention to the work taking place in laboratories today and tomorrow – medical science is the future of our healthy longevity.

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