Emory University scientists demonstrate that psilocybin—via its active metabolite psilocin—extends human cell lifespan by preserving telomeres and enhancing DNA repair, and increases survival by 30% in aged mice through reduced oxidative stress.

Key points

• Psilocybin’s active metabolite psilocin extends human skin and lung cell lifespan by over 50%, linked to enhanced DNA repair and telomere preservation.
• In aged mice, a regimen of 5 mg initial and 15 mg monthly psilocybin yields a 30% increase in survival and improved physical health biomarkers.
• Mechanistic studies reveal attenuation of oxidative stress, activation of DNA repair pathways, and maintenance of telomeric integrity as core anti‐aging effects.

Why it matters: These findings position psilocybin as a novel geroprotective candidate, offering multi‐targeted anti‐aging mechanisms beyond conventional senolytics and antioxidants.

Scientists from City of Hope and UCLA identify a novel age-specific adipocyte progenitor cell population (CP-As) that proliferates and differentiates into fat cells in middle-aged mice. Using single-cell RNA sequencing and in vivo lineage tracing, they pinpoint the LIFR signaling pathway as critical for CP-A mediated adipogenesis. Inhibiting LIFR signaling prevents visceral fat expansion, suggesting a promising strategy to mitigate age-related obesity and metabolic dysfunction.

Key points

• Discovery of CP-As: age-specific committed preadipocytes emerge in middle-aged adipose tissue.
• LIFR signaling: critical driver of CP-A proliferation and differentiation into new adipocytes.
• Lineage tracing & 3D APC transplants confirm autonomous fat-generating capacity of aged APCs.
• Single-cell RNA sequencing delineates gene expression profiles distinguishing CP-As from other APCs.
• Pharmacological LIFR inhibition prevents visceral fat expansion without affecting young APC adipogenesis.

Why it matters: By uncovering CP-As and their LIFR-driven adipogenesis, this work shifts the paradigm of age-related fat expansion, highlighting adipogenesis rather than hypertrophy as a major contributor. Targeting LIFR offers a precise therapeutic avenue to curb visceral obesity and metabolic disorders in middle-aged populations.