A new nanobody-based delivery system precisely targets healthy donor mitochondria to damaged neurons, cardiac cells, and other specific cell types — rescuing degenerating neurons in both a human optic-nerve-atrophy cell model and mice. Still preclinical, but a concrete step toward treating primary mitochondrial diseases like TK2 deficiency.
Read source →In a placebo-controlled RCT of 50 healthy middle-aged adults, 1,000 mg/day of urolithin A for 4 weeks expanded naive, less-exhausted CD8+ T cells and measurably increased mitochondrial biogenesis within those immune cells — a rare case of a supplement showing a measurable immune-aging effect this quickly. Conducted with the Buck Institute for Research on Aging.
Read source →The inflammaging signature derived from an Italian cohort (InCHIANTI) replicated in another industrialized population (Singapore), but largely vanished in two non-industrialized groups — the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. In those groups inflammation tracked infection burden rather than age, and showed little association with age-related disease. Suggests inflammaging may be substantially a byproduct of industrialized environments rather than a fixed feature of human aging.
Read source →A 4-month, placebo-controlled RCT (NCT03464500) found ~12% gains in muscle strength and improved mitochondrial biomarkers (lower plasma acylcarnitines and CRP) from the mitophagy-activating postbiotic Urolithin A.
Read source →The design paper for a randomized, double-blind, placebo-controlled trial testing whether clazakizumab, an antibody that blocks interleukin-6, can improve or slow decline in physical, cognitive and vascular function in adults aged 70 and over with low-to-moderate physical function. It is a direct test of the geroscience idea that targeting inflammation itself can extend healthspan. No results yet — this paper describes the rationale and protocol.
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