In mice, opioids and methamphetamine (but not natural rewards) trigger calcium influx through the mitochondrial calcium uniporter in dopamine-releasing nerve terminals, fueling the rapid ATP production that sustains drug-driven dopamine surges. Blocking this mitochondrial calcium channel genetically or pharmacologically reduced drug-induced dopamine release and addictive behavior without disrupting normal reward processing, pointing to it as a possible addiction drug target.
Read source →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 535 adults with overweight or obesity from the DiOGenes cohort, researchers split insulin resistance into its muscle and liver forms and profiled 1,128 plasma proteins. Muscle insulin resistance tracked 160 proteins dominated by inflammatory pathways, including IL-6 signalling; liver insulin resistance tracked 81 proteins centred on the complement system, with lower IGFBP-1, IGFBP-2, adiponectin and SHBG. Only 12 proteins overlapped. The authors argue this supports tissue-specific rather than one-size-fits-all interventions.
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 →Using bioinformatic and protein-docking analysis, researchers compared the mitochondrial-derived peptide humanin across mammals with different oxidative-stress profiles (deep-diving cetaceans, high-metabolism shrews, long-lived primates). Species under greater oxidative stress carried more structurally stable humanin variants, suggesting evolution has tuned the peptide's protective function and offering a template for designing humanin-based therapeutic analogs.
Read source →In transgenic mouse models, the mitochondrial-derived peptide MOTS-c boosted intrinsic muscle mitochondrial bioenergetics and lowered ROS-related oxidative damage — requiring both PGC-1α and AMPK signalling, without increasing raw mitochondrial volume. Animal data only; a human Phase 2a trial (MOTS-MET) for prediabetes began enrolling in 2026.
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.
Read source →Preclinical work showing MOTS-c, an mtDNA-encoded peptide, restores mitochondrial respiration and energy homeostasis in a type 2 diabetic cardiac model — building the mechanistic case for its "exercise mimetic" reputation.
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