ArticleAging cell2023
The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Distinct Transposable Element Transcript Patterns in Microglia Across Aging and Alzheimer's Disease.Aging cell · 2026Article
- Beyond biochemical cascades: novel bio-mechanical and epigenetic paradigms of glial SASP in brain aging.Metabolic brain disease · 2026Review
- Evidence of emerging transcriptome mediators of Alzheimer's disease in canine cognitive dysfunction.Brain pathology (Zurich, Switzerland) · 2026Article
- An FDA-Approved Tenofovir Alafenamide-Based Antiretroviral Therapy Reduces Biological Age in Healthy Adults: First Human Proof-of-Concept for Retrotransposon-Targeted Gerotherapeutics.medRxiv : the preprint server for health sciences · 2026Article
- Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026Review
- Implications of virus-induced stress granules in tauopathies.Translational neurodegeneration · 2026Review
- Review
- Epigenetic dysregulation of transposable elements in cognitive impairment and Alzheimer's disease.GeroScience · 2025Article
- Long-read sequencing reveals genomic and epigenomic variation in the dark genome of human Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Long-read sequencing-based analyses of the adult Drosophila brain transcriptome in physiological and pathological settings.BMC genomics · 2025Article
- Tripartite Interaction of Epigenetic Regulation, Brain Aging, and Neuroinflammation: Mechanistic Insights and Therapeutic Implications.Epigenomes · 2025Review
- Cytosolic DNA crosstalk in senescence: a new axis of inflammatory signaling?The EMBO journal · 2025Article
- Single-Cell Transcriptome Patterns of Transposable Elements in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Novel effects of reverse transcriptase inhibitor supplementation in skeletal muscle of old mice.Physiological genomics · 2025Article
- Immune modulation to treat Alzheimer's disease.Molecular neurodegeneration · 2025Review
- A Phase IIa clinical trial to evaluate the effects of anti-retroviral therapy in Alzheimer's disease (ART-AD).NPJ dementia · 2025Article
- RNA transcripts in salivary extracellular vesicle cargo isolated from aged populations.Frontiers in aging · 2025Article
- Repetitive element transcript accumulation is associated with inflammaging in humans.GeroScience · 2024Article
- Nanoligomers targeting NF-κB and NLRP3 reduce neuroinflammation and improve cognitive function with aging and tauopathy.Journal of neuroinflammation · 2024Article
- The reverse transcriptase inhibitor 3TC modulates hippocampal transcriptome signatures of inflammation in tauopathy model mice.Experimental gerontology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer's disease. Major hallmarks of brain aging include neuroinflammation/immune activation and reduced neuronal health/function. These processes contribute to cognitive dysfunction (a key risk factor for Alzheimer's disease), but their upstream causes are incompletely understood. Age-related increases in transposable element (TE) transcripts might contribute to reduced cognitive function with brain aging, as the reverse transcriptase inhibitor 3TC reduces inflammation in peripheral tissues and TE transcripts have been linked with tau pathology in Alzheimer's disease. However, the effects of 3TC on cognitive function with aging have not been investigated. Here, in support of a role for TE transcripts in brain aging/cognitive decline, we show that 3TC: (a) improves cognitive function and reduces neuroinflammation in old wild-type mice; (b) preserves neuronal health with aging in mice and Caenorhabditis elegans; and (c) enhances cognitive function in a mouse model of tauopathy. We also provide insight on potential underlying mechanisms, as well as evidence of translational relevance for these observations by showing that TE transcripts accumulate with brain aging in humans, and that these age-related increases intersect with those observed in Alzheimer's disease. Collectively, our results suggest that TE transcript accumulation during aging may contribute to cognitive decline and neurodegeneration, and that targeting these events with reverse transcriptase inhibitors like 3TC could be a viable therapeutic strategy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.