ArticleResearch square2024
Bidirectional relationship between epigenetic age and brain health events.
Article in Research square, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Accelerated biological aging based on DNA methylation clocks is a predictor of stroke occurrence: a systematic review and meta-analysis.Frontiers in neurology · 2025Pooled it
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Chronological age offers an imperfect estimate of the molecular changes that occur with aging. Epigenetic age, which is derived from DNA methylation data, provides a more nuanced representation of aging-related biological processes. This study examines the bidirectional relationship between epigenetic age and the occurrence of brain health events (stroke, dementia, and late-life depression). Using data from the Health and Retirement Study, we analyzed blood samples from over 4,000 participants to determine how epigenetic age relates to past and future brain health events. Study participants with a prior brain health event prior to blood collection were 4% epigenetically older (beta 0.04, SE 0.01), suggesting that these conditions are associated with faster aging than that captured by chronological age. Furthermore, a one standard deviation increase in epigenetic age was associated with 70% higher odds of experiencing a brain health event in the next four years after blood collection (OR 1.70, 95%CI 1.16-2.50), indicating that epigenetic age is not just a consequence but also a predictor of poor brain health. Both results were replicated through Mendelian Randomization analyses, supporting their causal nature. Our findings support the utilization of epigenetic age as a useful biomarker to evaluate the role of interventions aimed at preventing and promoting recovery after a brain health event.
Identifiers
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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 Socratic graph.