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As an addendum to the interesting telomerase, mitochondria and oxidative stress research noted at the Longevity Meme, here's another related paper from those posted to sci.life-extension today. This one looks at oxidative stress, the resulting damage to mitochondrial DNA, and its relation to the general state of your tissues:
Mitochondrial DNA (mtDNA) mutations appear to be associated with a wide spectrum of human disorders and proposed to be a potential contributor of aging. However, in an age-dependent increase of the common 4977bp deletion of human mtDNA still many unanswered questions remain.
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In vitro studies analyzing human normal cells transfected with telomerase (BJ-T) revealed that oxidative stress (OS) - a well accepted promoter of aging - induced 4977bp deletion and point mutations
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In conclusion, in heart tissue, the amount of the 4977bp deletion increased in an age-dependent manner and it was more detectable after the 4th decade of life, although there was some scatter in the data. Since, apoptosis was induced by the mitochondria-mediated pathway only in transformed cells, the role for apoptosis in normal tissue of the aging heart remains unclear.
This is what exploratory science looks like in a complex field - lots of teams prodding at the knowns and unknowns, and way more loose ends than people to make connections. As shown here, using telomerase on in vitro cell cultures doesn't seem to be a good way to understand what is going on in the body if - as other researchers claim - telomerase greatly influences the workings of oxidative stress and rates of mitochondrial DNA damage.
Still, there's no such thing as useless knowledge; it's all an advance. Yet we already know that technologies to replace damaged mitochondria could plausibly be developed in the same timeframe as the task of understanding what exactly all this biochemistry means. This, in essence, is the difference between engineering approaches and scientific approaches; you don't need full and complete knowledge to achieve a good result. In this case the good result would be healthy, undamaged mitochondria in old age, removing whatever contribution that damage makes to the aging process. While it would be beneficial to completely understand all the biochemistry and processes involved, researchers can achieve important medical goals without that full understanding - and in advance of it.
Technorati tags: aging, science
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Posted by Reason
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