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Chronic inflammation promotes NAD+ decline during aging

Senescent cells induce NAD+ decline via activation of CD8 macrophages


Key points from article :

NAD+ (nicotinamide adenine dinucleotide), a key metabolite to an efficient and healthy metabolism, declines with age.

Scientists have been unaware that whether the decline stems from decreased production of NAD+, a problem with “faucet,” or from its degradation, an issue akin to a “leaky sink”.

“Supplementation will be part of the equation, but filling the sink without dealing with the leak will be insufficient” - Eric Verdin.

Preliminary data suggests that blocking CD38 activity in older animals restores NAD+ levels in specific tissues.

Senescent cells spew pro-inflammatory proteins, called senescence-associated secretory phenotype (SASP).

“Inflammatory proteins in the SASP induce macrophages to proliferate, express CD38 and degrade NAD+” - Anthony Covarrubias, author.

"NAD+ is important to cellular health and we look forward to applying this discovery to stem the ravages of age-related disease” - Verdin.

Study by Buck institute published in Nature metabolism.

Mentioned in this article:

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Anthony J. Covarrubias

Assistant Professor at UCLA Life Sciences and David Geffen School of Medicine; Post doctor fellow at Verdin Lab, Buck Institute

Buck Institute

Independent biomedical research institute focused on aging

Eric Verdin

CEO & President at Buck Institute for Research on Aging

Nature Metabolism

Online journal Nature Metabolism is an online journal of Nature Research

Topics mentioned on this page:
NAD+, Inflammaging