Mesenchymal stem cells (MSCs) have been a topic of great interest in the last decade or so due to their ability to improve tissue regeneration merely by their presence and the secreted signals they give out.

Adult MSCs have traditionally been used for regenerative medicine with hit-and-miss results, depending on the quality and age of the harvested MSCs. It has been discovered in recent years that the efficacy of these cells greatly depends on how damaged by aging they are, which explains why MSC therapy sometimes works very well in one person but not so much in another.

However, what about aged cells that are reprogrammed back to pluripotency then guided into becoming mesenchymal stem cells through cellular reprogramming?

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Earlier this year, we launched a new webinar series where our monthly patrons, the Lifespan Heroes, are given the opportunity to join live discussion panels with the researchers who are working on solving aging.

Our April 8th, 2019 episode saw Dr. Mike Lustgarten, Dr. Amy Proal, and Dr. Cosmo Mielke join hosts Dr. Oliver Medvedik and Steve Hill for a discussion about the microbiome and how it relates to aging.

The webinar discusses gut flora and the pro-aging effects of immune system burden, the link between bacterial burden and inflammation, and exercise and nutrition. There was also plenty of discussion about the immediately available practical measures that can improve the gut microbiome and thus control weight and promote health.

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Rochester researchers have uncovered more evidence that the key to the “Fountain of Youth” may reside in a gene that is found to produce more potent proteins in species with longer lifespans. (Getty Images photo)

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Lying within our muscles are stem cells, invisible engines that drive the tissue’s growth and repair. Understanding the signal(s) that direct muscle stem cells to spring into action could uncover new ways to promote muscle growth. However, these mechanisms are poorly understood.

Now, scientists from Sanford Burnham Prebys have uncovered a molecular signaling pathway involving Stat3 and Fam3a proteins that regulates how muscle stem cells decide whether to self-renew or differentiate—an insight that could lead to muscle-boosting therapeutics for muscular dystrophies or age-related muscle decline. The study was published in Nature Communications.

“Muscle stem cells can ‘burn out’ trying to regenerate tissue during the natural aging process or due to chronic muscle disease,” says Alessandra Sacco, Ph.D., senior author of the paper and associate professor in the Development, Aging and Regeneration Program at Sanford Burnham Prebys. “We believe we have found promising drug targets that direct muscle stem cells to ‘make the right decision’ and stimulate muscle repair, potentially helping muscle tissue regeneration and maintaining tissue function in chronic conditions such as muscular dystrophy and aging.”

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On the degenerative disk disease and senescent cells from FightAging: “… It is just a pity that so few older people know this at the present time — the hundreds of millions worldwide who are suffering when perhaps they need not be…”

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At this point, I suspect it will surprise no-one who follows the field to learn that the accumulation of senescent cells is a significant cause of degenerative disc disease. The evidence from a mouse study that is provided in the open access paper here doesn’t quite rise to establishing that claim, but it is compelling nonetheless. Given the role of cellular senescence in arthritis, a disease of localized chronic inflammation, it is logical to also expect a role in the degeneration of intervertebral discs, as this is also a condition of aging in which inflammation seems important.

Senescent cells, even while present in only comparatively small numbers, generate a potent mix of molecules that spurs chronic inflammation and is destructive of surrounding tissue structure. Fortunately early senolytic compounds, those shown to destroy a sizable fraction of senescent cells cells in animal studies, are cheap and readily available to anyone willing to try this self-experiment. It is just a pity that so few older people know this at the present time — the hundreds of millions worldwide who are suffering when perhaps they need not be.

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