(Minor edits: comments directed to specific people have been knocked off.)
A cell needs to alter the methylation of the promoters for many genes in order to change the expression of many genes, so any change in the cell's internal or external environment to which the cell responds will lead to changes in its DNA methylation pattern; aging causes a massive amount of change in every cell, in its neighbors, and in the systemic environment (viz. parabiosis work, etc), so it's entirely to be expected that DNA methylation status will change sweepingly with age. Most obviously, when looking at blood cells: as "everybody knows," inflammation and oxidative stress in the blood rises with age for a variety of reasons (senescent cell accumulation, accumulation of cells homoplasmic for large mitochondrial DNA deletions, unresolved injury, age-related autoimmunity, rising burden of atherosclerotic lesions, etc, plus a variety of specific diseases of aging); oxidative stress both dysregulates expression of many genes, and elicits adaptive gene expression responses, while inflammation is itself mediated by gene expression (most clearly and consistently of interleukin-6). And we also know that levels of multiple hormones and other blood-borne signaling factors (TGF-β, GDF-11, etc) are also altered by aging damage; their signaling effects, too, are often mediated by changes in methylation of genes. At the same time, blood cells themselves are suffering damage that leads to changes in gene expression and accompanying methylation status, such as cellular senescence (driven by telomere attrition, oxidative stress, aberrant oncogene expression, etc) and involving in many cases demethylation of the p16 promoter) and the accumulation of anergic T-cells. (Contrariwise, there is now rather strong evidence that p16 hypermethylation can be detected in DNA in the blood of patients with some cancers (especially esophageal cancer): this is because tumor DNA escapes into the blood, and reflects the true mutations and epimutations that allow the cancer to escape senescence).
While some quick headline-generating results would be useful for fundraising, especially in the short term, the extension of lifespan of a model organism simply can't be achieved in the short term through the SENS "damage-repair" strategy. This is because multiple kinds of aging damage contribute to the degenerative aging process, and in order for the rejuvenation biotechnologies that SENS Research F
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