Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer
Open accessAbstract
A major goal in aging research is to improve health during aging. In the case of mice, genetic manipulations that shorten or lengthen telomeres result, respectively, in decreased or increased longevity. Based on this, we have tested the effects of a telomerase gene therapy in adult (1 year of age) and old (2 years of age) mice. Treatment of 1- and 2-year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging. Importantly, telomerase-treated mice did not develop more cancer than their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms using AAV vectors. Finally, telomerase-treated mice, both at 1-year and at 2-year of age, had an increase in median lifespan of 24 and 13%, respectively. These beneficial effects were not observed with a catalytically inactive TERT, demonstrating that they require telomerase activity. Together, these results constitute a proof-of-principle of a role of TERT in delaying physiological aging and extending longevity in normal mice through a telomerase-based treatment, and demonstrate the feasibility of anti-aging gene therapy.
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Systemic delivery of Tert lowers several senescence markers and ageing-related conditions and extends lifespan in wild-type mice, showing that telomeric DDR activation contributes to natural ageing.
“Systemic delivery of Tert reduces several senescence markers and ageing-related conditions and extends the lifespan of wild-type mice, thus demonstrating that telomeric DDR activation plays a role in natural ageing263.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [263]
The Results and Discussion report reduced p16 in most tissues, improved age-related health measures, and longer lifespan after AAV9-mTERT treatment of normal mice. The Discussion also links telomere-derived DNA damage to ageing, but the passages do not establish the more specific claim that activation of the telomeric DNA-damage response (DDR) contributes to natural ageing. Page numbers were not provided in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredControl AAV9 expressing GFP at the same dose used (2e12 vg/mouse) does not alter median lifespan when administered to 2-year-old mice.
“a previous report has demonstrated that control AAV9 expressing GFP at the same dose we used (2e12vg/mouse) does not alter median lifespan when administered to 2-year-old mice (Bernardes de Jesus et al., 2012)”
From Gene Therapy-Mediated Partial Reprogramming Extends Lifespan and Reverses Age-Related Changes in Aged Mice (2024) · cites this paper as Bernardes de Jesus et al., 2012
The Methods (Mice) and Results (AAV9-mediated expression) confirm that 2-year-old mice received control AAV9-GFP at 2 × 10¹² viral genomes per mouse. The Results (TERT-based gene therapy and longevity) compare lifespan in GFP-treated and untreated controls with TERT-treated mice, but do not report a direct median-lifespan comparison between GFP-treated and untreated mice. Thus, the assertion that GFP does not alter median lifespan is not established by our copy. (LLM, conf=0.86)
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Chou, Y., & Chen, Y. (2021) · Aging and Disease · doi:10.14336/ad.2020.0703 · Cited by 80 · see citing works
A new pleiotropic effect of statins in elderly: modulation of telomerase activity
Boccardi, V., Barbieri, M., Rizzo, M. R., Marfella, R., Esposito, A., Marano, L., & Paolisso, G. (2013) · The FASEB Journal · doi:10.1096/fj.13-232066 · Cited by 77 · see citing works
Distinguishing between driver and passenger mechanisms of aging
de Magalhães, J. P. (2024) · Nature Genetics · doi:10.1038/s41588-023-01627-0 · Cited by 76 · see citing works
- Authors
- Bernardes de Jesus, B., Vera, E., Schneeberger, K., Tejera, A. M., Ayuso, E., Bosch, F., & Blasco, M. A.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Universitat Autònoma de Barcelona (ES)
- Venue
- EMBO Molecular Medicine
- Published
- 2012-05-15
- Volume
- 4
- Issue
- 8
- Pages
- 691-704
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC3494070
- OpenAlex
- W2169621456
- Cited by
- 548
- References
- 79
- Citations by year
- 2026: 34 · 2025: 43 · 2024: 53 · 2023: 47 · 2022: 38 · 2021: 54 · 2020: 30 · 2019: 41 · 2018: 32 · 2017: 44 · 2016: 31 · 2015: 31 · 2014: 24 · 2013: 25 · 2012: 19
- FWCI
- 21.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- EMBO Molecular Medicine (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Dipòsit Digital de Documents de la UAB (Universitat Autònoma de Barcelona) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Funded Access
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Keywords
- telomerase, telomerase reverse transcriptase, gene therapy, aging, longevity, anti-aging, adeno-associated virus vectors, telomere length, cancer risk, insulin sensitivity, osteoporosis, neuromuscular coordination, aging biomarkers
- MeSH terms
- Dependovirus, Aging, Animals, Female, Genetic Vectors, Longevity, Male, Neoplasms, Genetic Therapy, Telomerase, Mice
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