Today I’ll point out a commentary on recent research in which a method of degrading mitochondrial function was shown to produce aspects of accelerated aging in mice. The commentary is somewhat more approachable than the paper it comments on. The challenge here is the same as in any form of research in which something vital is broken in animal biochemistry, and wherein the result looks a lot like a faster pace of aging. These forms of artificial breakage are almost never relevant to the understanding of normal aging; they create an entirely different state of metabolism and decline.
It is true that normal aging is a process of damage accumulation and reactions to that damage. But it is a specific mix of damage of specific types. That damage has the downstream consequence of loss of cell and tissue function, which in turn leads to the visible, well-known symptoms of aging and age-related disease. Near any form of significant damage and breakage in biochemistry will also lead to loss of cell and tissue function, however, even if it doesn’t normally occur in the wild. Very high levels of unrepaired nuclear DNA damage, far greater than exist
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