Two caveats govern every page on this site. (1) Telomere length is a contested aging biomarker — it is measured differently by different methods, varies between tissues, and "longer" is not straightforwardly "healthier"; changing a telomere-length or telomerase-activity number in a trial is not the same as slowing human aging. (2) Activating telomerase is not risk-free — telomerase expression is low in many differentiated normal tissues, while some normal proliferating cells can express it. Cancer can also use telomere maintenance; the included human records do not resolve long-term cancer risk from pharmacological activation. Tellingly, the FDA-approved telomerase inhibitor — imetelstat (RYTELO, 2024) — inhibits telomerase to treat cancer (lower-risk MDS), the opposite direction from the anti-aging "activation" narrative.
○ Evidence tier 5 — Animal lifespan study

Record verify: source publication identified; see evidence and limitations

DesignPreclinical AAV-TERT gene-therapy lifespan study (mouse)
PMID22585399
DOI10.1002/emmm.201200245
Citation statusOriginal publication identity matched by title, author and DOI; relevant full-text sections, results and limitations examined 2026-10-14.

Five-qualifier claim

Species / populationMice of both sexes on a >95%C57BL6 background, treated at420 or720days(called one-/two-year cohorts). At420days:14eGFP,21TERT,17catalytically inactiveTERT; at720days:14eGFP,23TERT. These are separate cohort denominators.
Exposure, route, scheduleOne tail-vein injection of 2 × 10^12 viral genomes per mouse of AAV9 expressing mouse TERT (AAV9-mTERT).
Comparator / durationAAV9-eGFP reporter-vector and untreated controls; survival follow-up with animals still alive censored in the Kaplan–Meier curves. The vector comparator was not an empty vector.
Endpoint / numeric resultMedian lifespan increased ~24% when treated at 1 year of age and ~13% when treated at 2 years, with delayed aging markers and NO reported increase in cancer incidence.
What it did NOT establishThis experiment tested mice, with mouse telomere biology and small cohorts. It does not establish human lifespan, disease benefit or safety. No observed increase in mouse tumors at necropsy is not a quantified assurance of human cancer safety.

Primary reference

https://doi.org/10.1002/emmm.201200245

Each identifier above was confirmed against the primary record; the citation status names the source and the date. An identifier that could not be confirmed is left empty and named as such in the record, never filled in from a secondary source.