Scientific Data — MethAgingDB: a comprehensive DNA methylation database for aging biology. MethAgingDB includes 93 datasets, with 11,474 profiles from 13 distinct human tissues and 1,361 profiles from 9 distinct mouse tissues. The database provides preprocessed DNA methylation data in a consistent matrix format, along with tissue-specific DMSs and DMRs, gene-centric aging insights, and an extensive collection of epigenetic clocks. Together, MethAgingDB is expected to streamline aging-related epigenetic research and support the development of robust, biologically informed aging biomarkers.
Psilocybin improved longevity and health markers in mice and cells. The findings reveal unexpected systemic benefits. As the anti-aging industry, fueled by optimism and a flood of supplements, generated more than $500 million in revenue last year, scientists at Emory University discovered a compo
Brian Kennedy is a renowned biologist, leader in aging research, & director of the Center for Healthy Longevity at the National University of Singapore. In this episode, Brian shares insights from ongoing human aging studies, including clinical trials of rapamycin & how dosing strategies, timing, & exercise may influence outcomes. He presents two key models of aging—one as a linear accumulation of biological decline & the other as an exponential rise in mortality risk—& explains why traditional models of aging fall short. He also explains why most current aging biomarkers lack clinical utility & describes how his team is working to develop a more actionable biological clock. Additional topics include the potential of compounds like alpha-ketoglutarate, urolithin A, & NAD boosters, along with how lifestyle interventions—such as VO2 max training, strength building, & the use of GLP-1 & SGLT2 drugs—may contribute to longer, healthier lives.
0:00:00-Intro. 0:01:15-Brian’s journey from the Buck Institute to Singapore, & the global evolution of aging research. 0:09:12-Rethinking the biology of aging. 0:14:13-How inflammation & mTOR signaling may play a central, causal role in aging. 0:18:00-Biological role of mTOR in aging, & the potential of rapamycin to slow aging & enhance immune resilience. 0:23:32-Aging as a linear decline in resilience overlaid with non-linear health fluctuations. 0:36:03-Speculating on the future of longevity: slowing biological aging through noise reduction & reprogramming. 0:42:18-The role of the epigenome in aging, & the limits of methylation clocks. 0:47:14-Balancing the quest for immortality with the urgent need to improve late-life healthspan. 0:52:16-Comparing the big 4 chronic diseases: which are the most inevitable & modifiable? 0:57:27-Exploring potential benefits of rapamycin: how Brian is testing this & other interventions in humans. 1:09:14-Testing alpha-ketoglutarate (AKG) for healthspan benefits in aging [1:01:45]; 1:13:41-Exploring urolithin A’s potential to enhance mitochondrial health, reduce frailty, & slow aging. 1:17:35-Potential of sublingual NAD for longevity. 1:26:50-Other interventions that may promote longevity: spermidine, 17 HRT, & more. 1:34:33-Biological aging clocks, clinical biomarkers, & a new path to proactive longevity care. 1:45:01-Evaluating rapamycin, metformin, & GLP-1s for longevity in healthy individuals. 1:51:19-Why muscle, strength, & fitness are the strongest predictors of healthspan. 1:53:37-Why combining too many longevity interventions may backfire. 1:56:06-How AI integration could accelerate breakthroughs in aging research. 2:02:07-Need to balance innovation with safety in longevity clinics. 2:10:50-Peter’s reflections on emerging interventions & the promise of combining proven aging compounds.
——- About:
The Peter Attia Drive is a deep-dive podcast focusing on maximizing longevity, & all that goes into that from physical to cognitive to emotional health. With over 90 million episodes downloaded, it features topics including exercise, nutritional biochemistry, cardiovascular disease, Alzheimer’s disease, cancer, mental health, & much more.
Peter Attia is the founder of Early Medical, a medical practice that applies the principles of Medicine 3.0 to patients with the goal of lengthening their lifespan & simultaneously improving their healthspan.
Despite significant advances in aging research, translating these findings into clinical practice remains a challenge. Aging is a complex, multifactorial process shaped by many factors including genetic, metabolic, and environmental factors. While medical advancements have extended lifespan, healthspan remains constrained by cellular senescence, telomere attrition, and systemic inflammation—core hallmarks of biological aging. However, emerging evidence suggests that telomere dynamic is not inevitable but can be influenced by oxidative stress, lifestyle choices, and metabolic regulation. This review examines how telomere-based biomarkers and metabolic interventions can drive personalized longevity medicine, enabling targeted strategies to delay aging.
A surprising new study has uncovered over 200 misfolded proteins in the brains of aging rats with cognitive decline, beyond the infamous amyloid and tau plaques long blamed for Alzheimer’s. These shape-shifting proteins don’t clump into visible plaques, making them harder to detect but potentially just as harmful. Scientists believe these “stealth” molecules could evade the brain’s cleanup systems and quietly impair memory and brain function. The discovery opens a new frontier in understanding dementia and could lead to entirely new targets for treatment and prevention.
Degradation of proteostasis, mitochondrial function, and cellular stress resistance results in a build-up of damaged proteins, oxidative insult, and chronic inflammation, characteristic of aging. CHIP is essential for maintaining protein quality control and cellular homeostasis by having dual E3 ubiquitin ligase and co-chaperone activities. CHIP facilitates proteostasis by maintaining proteostasis in misfolded, aggregated proteins by promoting their degradation. Mitochondrial dysfunction, oxidative imbalance, and cellular senescence are caused by its age-associated decline and contribute to neurodegenerative, cardiovascular, and oncogenic disease pathogenesis. Examples of recent pharmacological and gene-based strategies to correct CHIP and restore stress resilience have been made.
Antler blastema progenitor cells (ABPCs) are a distinct population of skeletal mesenchymal stem cells found in regenerating deer antlers, with strong stemness and renewal capacity in vitro. Stem cell-derived extracellular vesicles (EVs) are emerging as potential therapeutic candidates that can mediate donor cells’ beneficial effects. Here, we tested the effects of ABPC-derived EVs (EVsABPC) on aging in mice and rhesus macaques (Macacamulatta). We identified a variety of unique factors in EVsABPC and showed that in vitro, EVsABPC attenuated phenotypes of senescence in bone marrow stem cells. In aged mice and macaques, EVsABPC substantially increased femoral bone mineral density. Further, intravenous EVsABPC improved physical performance, enhanced cognitive function and reduced systemic inflammation in aged mice, while reversing epigenetic age by over 3 months. In macaques, EVABPC treatment was also neuroprotective, reduced inflammation, improved locomotor function and reduced epigenetic age by over 2 years. Our findings position ABPCs as an emerging and practical source of EVs with translational value for healthy aging interventions.
Inspired by the regenerative capacity of deer antlers, Hao and colleagues report that antler blastema progenitor cell-derived extracellular vesicle treatment counteracts bone loss and epigenetic aging and is neuroprotective in mice and macaques.
