Telomerase reverse transcriptase preserves neuron survival and cognition in Alzheimer’s disease models
Open accessAbstract
Amyloid-induced neurodegeneration plays a central role in Alzheimer's disease (AD) pathogenesis. Here, we show that telomerase reverse transcriptase (TERT) haploinsufficiency decreases BDNF and increases amyloid-β (Aβ) precursor in murine brain. Moreover, prior to disease onset, the TERT locus sustains accumulation of repressive epigenetic marks in murine and human AD neurons, implicating TERT repression in amyloid-induced neurodegeneration. To test the impact of sustained TERT expression on AD pathobiology, AD mouse models were engineered to maintain physiological levels of TERT in adult neurons, resulting in reduced Aβ accumulation, improved spine morphology, and preserved cognitive function. Mechanistically, integrated profiling revealed that TERT interacts with β-catenin and RNA polymerase II at gene promoters and upregulates gene networks governing synaptic signaling and learning processes. These TERT-directed transcriptional activities do not require its catalytic activity nor telomerase RNA. These findings provide genetic proof-of-concept for somatic TERT gene activation therapy in attenuating AD progression including cognitive decline.
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Tert transcriptional activation in transgenic 3xTg-AD mice reduces abnormal intracellular Aβ staining in the CA1 region and upregulates genes involved in synaptic signaling and neuronal survival.
“In line with our data, a very recent study has shown that Tert transcriptional activation in transgenic 3xTg-AD mice (which carry two FAD mutations together with a mutation of the MAPT gene [88]) reduces abnormal intracellular Aβ staining in the CA1 region and upregulates genes involved in synaptic signaling and neuronal survival [106].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [106]
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From Lab Bench to Hope: Emerging Gene Therapies in Clinical Trials for Alzheimer’s Disease
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“Research in both cellular and animal models has demonstrated the neuroprotective effects of TERT in reducing brain injury [67, 72, 76, 77].”
InfluentialExploring the Causal Relationship Between Telomere Biology and Alzheimer’s Disease
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“However, it can also regulate transcription via its non-catalytic interaction with other enzymes, upregulating the expression of neurotrophic factors, and thus preserving cognitive function [56, 57].”
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“Moreover, TERT gene therapy enhances learning pathway networks in human neurons (Shim et al., 2021).”
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“Similarly, modest and complete Tert deficiency differentially regulates the expression of numerous genes involved in amyloid precursor proteinmetabolic processes in the brain of Tert−/− and Tert+/− mice, respectively (Shim et al., 2021).”
BackgroundGenetic and epigenetic alterations in aging and rejuvenation of human
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A Unified Model of Age-Related Cardiovascular Disease
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Telomeres: Dysfunction, Maintenance, Aging and Cancer
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“Cultured hippocampal 5xFAD neurons at 10–13 days in vitro exhibit neither severe amyloid pathology, due to limited time to accumulate human APP and PS1 transgenes, nor detectable level of amyloids [6].”
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“Interestingly, TERT activation reduces amyloid pathology, restores spine morphology, and improves learning and memory in AD [370].”
Fatigue in Alzheimer’s disease: biological basis and clinical management—a narrative review
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“…survival is reduced in AD due to the induction of neuronal apoptosis, necrosis, ferroptosis, and pyroptosis by Aβ and tau protein, and associated neuroinflammation, oxidative stress, ER stress, and mitochondrial dysfunction (Mangalmurti and Lukens 2022; Shim et al. 2021; Mohamed and Bars 2024 ).”
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“In neurons, H3K9me3 results in TERT repression (35).”
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The Telomerase Connection of the Brain and Its Implications for Neurodegenerative Diseases
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Haploinsufficiency and Alzheimer’s Disease: The Possible Pathogenic and Protective Genetic Factors
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“TERT induction reduced amyloid peptide levels in neurons of AD mouse models and improved cognition via the beta-catenin/TCF7 complex [136].”
Clinical gene therapy development for the central nervous system: Candidates and challenges for AAVs
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Unraveling the molecular mechanisms of aluminium chloride-induced Alzheimer’s disease
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“Consequently, this combined model of senescence and tauopathy could serve as a valuable preclinical research model to more accurately recapitulate the extent of neuronal death observed in tau-related human diseases and evaluate potential therapeutic targets.”
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“…HP neurons, which corresponds to increased CME and APP production in WT neurons, and tracks with accumulation of A β oligomers in 5xFAD primary neurons seen after 14 days (Shim et al., 2021), could also function as a compensatory mechanism to reduce CME and A β and prevent subsequent synaptic loss.”
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“…involving mice, researchers demonstrated that the enforced expression of neuronal TERT through crossbreeding with an AD amyloid mouse model resulted in decreased amyloid deposition, suppressed activation of astrocytes and microglia, increased dendritic spines, and improved learning and memory 65 .”
Sharma, H. S., Muresanu, D. F., Nozari, A., Lafuente, J. V., Buzoianu, A. D., Tian, Z. R., Huang, H., Feng, L., Bryukhovetskiy, I., Manzhulo, I., et al. (2023) · Advances in neurobiology · doi:10.1007/978-3-031-32997-5_4 · Cited by 5 · see citing works
Gene expression in mice with endothelium-specific telomerase knockout
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“…telomerase activators exert potent non-canonical, neuroprotective effects by upregulating gene networks governing synaptic signaling and cognition [66], enhancing the expression of neurotrophins (e.g., BDNF) and neuronal plasticity genes (GAP43, NeuN, SYP) [67], promoting the autophagic clearance…”
Viral vectors in neurodegenerative diseases: immune responses and therapeutic applications
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“Notably, in the brain, TERT primarily exerts non-telomeric functions, including regulation of gene expression, synaptic signaling, and neurotrophic support [131].”
InfluentialZheng, Z., Chen, C., Zhu, S., Zhu, X., Tu, H., Ding, X., Xia, T., & Gu, X. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115543 · Cited by 3 · see citing works
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Detection and pharmacokinetics of licochalcone A in brains of neuroinflammatory mouse model
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Molecular Determinants of Neurocognitive Deficits in Glioma: Based on 2021 WHO Classification
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“Furthermore, it has been discovered that in mouse models, TERT maintenance leads to the enhancement of the gene network responsible for controlling synaptic signaling and learning processes, which are significant for the preservation of cognitive functions (Shim et al. 2021).”
BackgroundSelf-citationZhang, Y., He, J., Xiang, L., Tang, X., Wang, S., Li, A., Wang, C., Li, L., & Zhu, B. (2024) · Current Pharmaceutical Design · doi:10.2174/0113816128288504240321041408 · Cited by 3 · see citing works
Epigenetic Control of TERRA by FTSJ3 is Critical for Telomerase-Driven CancersPreprint
Price, J. D. W., Vizeacoumar, F. S., Abuhussein, O., Maranda, V., Zhang, Y., Adachi, H., Kyrylenko, L., Pozzo, A. R., Dong, H., Gong, L. H., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.26.634101 · Cited by 3 · see citing works
Self-citationCounteracting Alzheimer’s disease via somatic TERT activation
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Арифметика DR+Preprint
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“In AD, downregulation of telomerase activity may lead to shortening of neuronal telomeres and accelerated cellular senescence and death [25].”
Self-citationAge-related disease: Cardiovascular system
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Noncoding RNAs and RNA Epigenetics in Brain Aging
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Link Between Shortened Telomeres and Brain Pathology Mitigated by Modifiable Risk Factors
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ARMH4 accelerates aging by maintaining a positive-feedback growth signaling circuit
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“Studies on AD mouse models showed that sustained physiological expression of telomerase reverse transcriptase in adult neurons resulted in decreased amyloid aggregates and improved cognition [24].”
Relationship between hTERT levels and oxidative stress in epilepsy patients
Üremi̇ş, M. M., Berktaş, D. T., Üremiş, N., & Tolun, F. İ. (2026) · Epilepsia Open · doi:10.1002/epi4.70165
Blázquez-Moreno, A., Orgaz, L., Rodríguez-Moreno, E., Asensio, A., Marsal, M. F., Mantecón, L., Infante, C., Samper, E., & Flemetakis, E. (2026) · Nutrition and Health · doi:10.1177/02601060261431078
Overview of hallmarks of aging
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“11 25 26 The reactivation of TERT expression through gain- of-function mutations in its promoter is a common event in the malignant transformation of various human cancers.”
Epigenetic control of telomeric RNA maintains heterochromatin in telomerase-driven cancers
Price, J. D. W., Vizeacoumar, F. S., Abuhussein, O., Maranda, V., Zhang, Y., Adachi, H., Nguyen, K., Kyrylenko, L., Pozzo, A. R., Dong, H., et al. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-026-02750-0 · Cited by 3 · see citing works
“In parallel, a broad signaling module was enriched, recapitulating known connections between hTERT and NF-κ B signaling 19 , Wnt signaling 20,21 , and Rho GTPases 22 (Fig.”
Self-citationAging impact on canine extracellular vesicles production, size, and miRNA content
Marina, C. L., Greuel, A. M., Las-Casas, L. D. O., Lopes-Gomes, E., Ferrari, S. S. D. A. R., Rodrigues, M. L., Reis, F. C. G., Bocca, A. L., Titze-de-Almeida, S. S., Resende, F. F. B., et al. (2026) · Veterinary Research Communications · doi:10.1007/s11259-026-11354-6
“Normally, this process is delayed by telomerase and failure in this enzyme leads to accelerated aging and neurodegenerative disorders such as Alzheimer’s disease (Shim et al. 2021, Hipp et al. 2019 , Pievani et al. 2014, Martínez-CuNoemí Rueda et al. 2020, Zhang et al. 2025).”
Anthocyanins and Aging Intervention: Mechanisms and Prospects
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Positioning TERT at the apex of aging
DePinho, R. A. (2026) · Nature Aging · doi:10.1038/s43587-026-01179-y
“Related studies have reported complementary findings, including lifespan and functional benefits after TERT gene delivery in adult and old mice 9,41 , as well as neuroprotective effects in models of neurode-generation 11 .”
InfluentialSelf-citationFatima, S. U. K., Jabber, A., Khanam, M. H., Khan, J., Talukder, M. M., & Hasnat, M. A. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261476085
“8,37 Starting from a priori universe of telomere-associated genes, we identi fi ed a 38-gene AD-linked signature in the hippocampus and revealed that these genes segregate into two coherent co-expression modules.”
InfluentialUnderstanding extracellular vesicles in antiaging
Ahmad, P., Estrin, N. E., Sculean, A., & Miron, R. J. (2026) · Periodontology 2000 · doi:10.1111/prd.70070
Telomerase reverse transcriptase as a core regulator of brain health
Shim, H. S., & DePinho, R. A. (2026) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2026.08.003
Self-citationHuang, J., Ji, L., Jin, H., Shi, Z., Song, X., Cai, Y., & Tong, X. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103398
TERT is a therapeutic target for tertiary stroke prevention
Luo, S., Gu, T., Liang, M., Zhou, Y., Su, G., Xie, X., Yang, W., Chen, M., & Tsang, C. K. (2026) · Journal of Advanced Research · doi:10.1016/j.jare.2026.10.016
Mechanisms of brain aging. A review: Part I
Berns, S. A., Веремеев, А. В., Lobachev, I. M., Shirshov, A. V., Korshikova, E. A., Timofeev, Y. S., Ринатовна, Г. И., Almazova, I. I., & Drapkina, O. M. (2026) · CARDIOVASCULAR THERAPY AND PREVENTION · doi:10.15829/10.15829/1728-8800-2026-4986
- Authors
- Shim, H. S., Horner, J. W., Wu, C.-J., Li, J., Lan, Z. D., Jiang, S., Xu, X., Hsu, W.-H., Zal, T., Flores, I. I., Deng, P., Lin, Y.-T., Tsai, L.-H., Wang, Y. A., & DePinho, R. A.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Massachusetts Institute of Technology (US)
- Corresponding author
- Wang, Y. Alan
- DePinho, Ronald A.
- ORCID
- Venue
- Nature Aging
- Published
- 2021-12-20
- Volume
- 1
- Issue
- 12
- Pages
- 1162-1174
- ISSN
- 2662-8465 (ISSN-L)
- PMC
- PMC8759755
- OpenAlex
- W4200501792
- Cited by
- 73
- References
- 81
- Citations by year
- 2026: 18 · 2025: 17 · 2024: 16 · 2023: 15 · 2022: 5 · 2021: 2
- FWCI
- 5.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-sa)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA231349, R01CA084628, P30CA016672)
- National Center for Research Resources (S10RR029552)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- telomerase reverse transcriptase, Alzheimer's disease, amyloid-beta, brain-derived neurotrophic factor, epigenetic repression, β-catenin, RNA polymerase II, synaptic signaling, cognitive decline, gene therapy, neuronal survival, preclinical models
- MeSH terms
- Alzheimer Disease, Animals, Cognition, Humans, Neurons, Amyloid beta-Peptides, Telomerase, Mice
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