In this episode of Longevity Papers, we analyze five standout papers from longevitypapers.com covering the past four weeks of longevity research (February-March 2026): 1) Microbiome depletion rejuvenates the aging brain (Gasperini, Holton, Limone et al., Harvard University, February 15, 2026, bioRxiv, https://www.biorxiv.org/content/10.64898/2026.02.13.705770v1 ) - Antibiotic-induced microbiome depletion in aged mice triggers widespread brain rejuvenation including improved neurogenesis, myelination, vascular density, and memory. The aged gut microbiome drives brain aging through eotaxin-1 (CCL11) - the same factor found elevated in old blood in the classic heterochronic parabiosis studies. Inhibiting eotaxin-1 alone was sufficient to reverse multiple brain aging hallmarks. 2) Transplanting ANXA1- CD8+ Naive T cells Delay Aging Through Senolysis (Wu, Guo, Zhang et al., Shanghai Jiao Tong University, February 23, 2026, bioRxiv, https://www.biorxiv.org/content/10.64898/2026.02.21.707223v1 ) - Monthly transfer of ANXA1-deficient CD8+ naive T cells into aged mice extended median lifespan by more than 30 weeks and improved cardiac function, bone density, and motor coordination. The aging immune system fails to clear senescent cells because CD8+ naive T cells accumulate an ANXA1+ senescent-like subpopulation. Removing this subpopulation restores immune senolysis. 3) Organism-wide cellular dynamics and epigenomic remodeling in mammalian aging (Lu, Zhang, Xu et al., Rockefeller University, February 26, 2026, Science, https://www.science.org/doi/10.1126/science.adw6273 ) - Landmark single-cell chromatin atlas of approximately 7 million cells across 21 mouse tissues at three ages reveals that 25% of cell types show dramatic age-related population shifts including loss of kidney podocytes, muscle tenocytes, and lung aerocytes. Critically, 40% of aging dynamics differ between males and females. 4) The glycolytic metabolite phosphoenolpyruvate restricts cGAS-driven inflammation to promote healthy aging (Song, Hu, Zhang et al., Nanhu Laboratory, March 7, 2026, Nature Aging, https://www.nature.com/articles/s43587-026-01087-1 ) - PEP, a normal glycolytic intermediate, is an endogenous cGAS inhibitor that declines with age, unleashing cGAS-STING-driven inflammaging. Restoring PEP before its natural age-related decline promotes healthy aging in mice and alleviates Alzheimer's disease symptoms. 5) Cellular Aging Signatures in the Plasma Proteome Record Human Health and Disease (Ding, Bot, Chen et al., Stanford University, February 12, 2026, bioRxiv, https://www.biorxiv.org/content/10.64898/2026.02.10.704909v1 ) - The largest plasma proteomics aging study ever: 60,000 individuals, 7,000+ proteins, biological age estimates for 40+ cell types. APOE4 carriers show older astrocytes but younger macrophages, directly linking cell-type-specific aging to Alzheimer's disease risk. Cellular aging signatures predict incident disease and mortality over 15 years of follow-up. This podcast is AI generated and may contain errors.