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Autophagy maintains stemness by preventing senescence.

I think this article is remarkable; I spent over an hour reading it. That autophagy can reverse senescence integrates observations about CR, IF, and rapamycin extending lifespan in some organisms. Here, they studied dysfunction of autophagy (and it's enhancement/reversal) in geriatric satellite cells in mice. Re: lysosomal dysfunction from the full-text: "Geriatric satellite cells also showed increased co-localization of p62–ubiquitin aggregates in non-degraded autophagosomes (Fig. 2b). As p62 marks damaged organelles for degradation by selective autophagy, whereas ubiquitin marks substrates for their degradation by either the ubiquitin–proteasome system (UPS) or selective autophagy, the increased signal of both proteins and their co-localization demonstrates that the autophagic defect in these cells is due, at least in part, to a block in autophagosomal or lysosomal clearance.....Thus, loss of autophagy with ageing may be the cause underlying the age-associated numerical decline in muscle stem cells7,8,10–13.....". They also talk about lysosomal dysfunction causing increased ROS, which if addressed, can also recover satellite cell function. From the full-text: "Trolox treatment
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Paracrine effects of haematopoietic cells on human mesenchymal stem cells.

If I'm understanding this correctly, they're supposing that age-related changes in HSC protein expression may have senescence-inducing effects on MSC. If this is correct, it may be that correcting age-related changes in HSC paracrine protein expression may improve MSC function. Moreover, if these HSC paracrine factors affect MSC senescence, it could be that they effect senescent-type changes in other cell types.
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Are there roles for brain cell senescence in aging and neurodegenerative disorders?

I scanned the full-text, and found this to be a useful reference on senescent cell biology. As for the possibility of senescent neurons and glia, here is a summary quote from the full-text: "In both AD and PD there is evidence for several CS hallmarks including: aberrant expression of cell cycle proteins (Luth et al. 2000), nuclear abnormalities (Metuzals et al. 1988), lysosomal and autophagic dysfunction (Nixon 2013), impaired mitochondrial function that leads to enhanced ROS generation (Mattson et al. 1999), and production of pro-inflammatory cytokines such as IL-6 (Wood et al. 1993). While it is still possible that this collection of senescent-like phenotypes found in CNS cell populations of aging, AD and PD brains could all be due to unique aspects of disease etiology, it is suggestive that CS does indeed take place in the CNS during normal aging as well as in age-related disease."
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Free report on high blood pressure

The American Heart Association estimates more than 100 million Americans have high blood pressure, also known as “hypertension”. Learn more about the cause of high blood pressure and how you can reverse it in our free report.

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Biomarker levels predict the risk of early death—and we can change them! Learn about some important longevity biomarkers in our free report.

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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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