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Somatic mutant clones colonize the human esophagus with age.

This looks like an interesting report of the accumulation of nuclear DNA mutants in human esophageal epithelium. This group found that somatic mutations accumulated during human aging in this tissue, with "a strong positive selection of clones carrying mutations in 14 cancer genes", with mutations in NOTCH1 and TP53 having relatively high prevalence (even higher than the rates found in esophageal cancers). These results make me wonder about the dynamics of cancer-related gene mutations during human aging. I wonder whether the age-related increase in cancer incidence is caused by the metabolic-abuse-area-under-the-curve associated with a longer time alive (living longer = more damage), or whether there is some positive selection process for cancer-associated gene mutations, or maybe the increased cancer incidence is caused mostly by a decline in immune function, or perhaps the explanation varies by cancer type.
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Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation.

I wonder if readers on this distribution list have already seen this association between mtDNA double-strand breaks and demyelination. If I recall correctly, I thought I've seen demyelination observed to be age-related. If so, could mtDNA damage be a primary cause? Or is this a case of there being many ways to induce a given dysfunction, and that this particular one is not likely to be occurring during human aging?
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The ageing genome, clonal mosaicism and chronic disease.

Clonal mosaicism refers to when one cell experiences a mutation, then divides a sufficient number of times such that this new mutation can be detected among cells without that mutation. These authors review this topic, and its potential relevance to chronic disease, including cancer. This topic seems relevant to the question of whether nuclear DNA damage (in this case, mutation) matter during a normal human lifespan.
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The cell fate: senescence or quiescence.

This appears to be an interesting review article about cellular senescence, which also contrasts senescence with quiescence. Included in the discussion are pathways and mediators of both quiescence and senescence.
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Do DNA Double-Strand Breaks Drive Aging?

I'm pretty confident I have seen other writings by Vijg about the possibility of DNA double-strand breaks being a fundamental type of "damage" in aging, potentially causing various aspects of declining health with advancing age. I'm not sure whether he says anything new here; I'll leave it up to readers following this space to decide.
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Free report on high blood pressure

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An estimated 50% of American adults have either prediabetes or type 2 diabetes. Learn more about the cause of type 2 diabetes, prediabetes, insulin resistance, and how to reverse them in our free report.

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