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This is of interest because it provides a much better methodology for lengthening telomeres, with more control than genetic engineering, and therefore a faster path to establishing why telomerase therapy extends life in mice.

Average telomere length in tissue is a measure of health in general: since telomere length decreases with each cell division it is a proxy for some combination of cell division rates and rate of influx of fresh new cells with long telomeres provided by the stem cell population maintaining a tissue. Since average telomere length is often measured in white blood cells it goes up and down with health and generally downward with age. Stem cell activity declines with age, so this shouldn't be surprising.

Lengthening telomeres via telomerase may extend life in mice for any number of reasons, some of which actually have nothing to do with telomeres. Telomerase, like all biomolecules, has a lot of roles, not all of which are fully understood. Alternative and more controllable methods of lengthening telomeres should help narrow down what is going on in those studies. Is it greater stem cell activity, something to do with telomerase influencing mitochondrial function, something completely different?

In general if you're thinking of aging as accumulated molecular damage, telomere shortening looks like a consequence not a root cause. It may cause further issues itself, but targeting it is probably not as effective as going for the actual root causes that lead to it. The interesting question is why telomerase therapy does do comparatively well in extending life in mice.