A team at Baylor College of Medicine reports that psilocybin preserves telomere length, delays cellular senescence, and elevates SIRT1 expression in human fibroblasts, yielding up to 57% lifespan extension in vitro and enhanced survival and fur quality in aged mice.
Key points
Psilocybin preserves telomere length and delays replicative senescence in human fibroblasts.
10 μM psilocin treatment elevates SIRT1 expression and enhances DNA damage responses.
Systemic administration to aged mice improves survival rates and fur quality, indicating geroprotective effects.
Why it matters:
By revealing psilocybin's capacity to target cellular aging pathways, this research opens avenues for novel geroprotective therapies beyond neuropsychiatric applications.
Q&A
What are telomeres?
How does SIRT1 influence aging?
Are psilocybin’s effects limited to the brain?
What safety considerations exist for psilocybin use?
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Academy
Telomeres and Aging
Telomeres are protective caps composed of repetitive nucleotide sequences located at the ends of chromosomes. They safeguard genetic information by preventing the collapse of chromosomal ends and the erroneous activation of DNA repair pathways. Each time a cell divides, conventional DNA polymerase cannot fully replicate the very ends of linear chromosomes, leading to progressive telomere shortening. Over time, critically short telomeres trigger cellular senescence or apoptosis, hallmark processes in organismal aging.
Telomere shortening is strongly associated with age-related diseases, including cardiovascular disorders, neurodegeneration, and impaired tissue regeneration. By preserving telomere length, cells can maintain proliferative capacity and genomic stability. Strategies to maintain or elongate telomeres are under investigation for their potential to delay aging and extend healthspan.
- Structure: Telomeres consist of tandem repeats of the sequence TTAGGG in vertebrates, bound by a protein complex called shelterin.
- Function: Shelterin prevents chromosome ends from being mistaken for DNA breaks, regulating repair and recombination.
- Shortening Mechanism: The end-replication problem and oxidative damage accelerate telomere attrition, linking cellular stress to aging.
SIRT1: A Key Longevity Protein
Sirtuin 1 (SIRT1) is an enzyme from the sirtuin family that requires nicotinamide adenine dinucleotide (NAD+) to remove acetyl groups from proteins, including histones and transcription factors. This deacetylation modulates chromatin structure and gene expression, influencing pathways related to DNA repair, inflammation, metabolism, and stress resistance. SIRT1 activation is associated with increased lifespan in multiple organisms and protective effects against metabolic and neurodegenerative diseases.
SIRT1 regulates critical cellular processes:
- Genome Stability: Enhances DNA repair by deacetylating repair proteins and histones at damage sites.
- Metabolic Homeostasis: Controls transcription factors like PGC-1α, affecting mitochondrial biogenesis and energy metabolism.
- Inflammation Modulation: Suppresses pro-inflammatory gene expression by targeting NF-κB signaling.
- Cell Survival: Coordinates stress responses under caloric restriction and oxidative stress, promoting cell viability.
Together with telomere preservation, SIRT1 activation represents a synergistic strategy to combat cellular aging. Compounds like psilocybin that influence both telomere maintenance and sirtuin pathways are promising candidates in the development of geroprotective therapies.
