Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression
Abstract Chronological age is an imperfect estimate of molecular aging. Epigenetic age, derived from DNA methylation data, provides a more nuanced representation of aging-related biological processes. We examine the bidirectional relationship between epigenetic age and brain health events (stroke, d...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2025-02-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-024-54721-0 |
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| author | Cyprien A. Rivier Natalia Szejko Daniela Renedo Santiago Clocchiatti-Tuozzo Shufan Huo Adam de Havenon Hongyu Zhao Thomas M. Gill Kevin N. Sheth Guido J. Falcone |
| author_facet | Cyprien A. Rivier Natalia Szejko Daniela Renedo Santiago Clocchiatti-Tuozzo Shufan Huo Adam de Havenon Hongyu Zhao Thomas M. Gill Kevin N. Sheth Guido J. Falcone |
| author_sort | Cyprien A. Rivier |
| collection | DOAJ |
| description | Abstract Chronological age is an imperfect estimate of molecular aging. Epigenetic age, derived from DNA methylation data, provides a more nuanced representation of aging-related biological processes. We examine the bidirectional relationship between epigenetic age and brain health events (stroke, dementia, late-life depression) using data from 4,018 participants. Participants with a prior brain health event are 4% epigenetically older (β = 0.04, SE = 0.01), indicating these conditions are associated with accelerated aging beyond that captured by chronological age. Additionally, a one standard deviation increase in epigenetic age is associated with 70% higher odds of experiencing a brain health event in the next four years (OR = 1.70, 95% CI = 1.16–2.50), suggesting epigenetic age acceleration is not just a consequence but also a predictor of poor brain health. Mendelian Randomization analyses replicate these findings, supporting their causal nature. Our results support using epigenetic age as a biomarker to evaluate interventions aimed at preventing and promoting recovery after brain health events. |
| format | Article |
| id | doaj-art-50e3de8cd0b549c19e5938b04d6f2760 |
| institution | Kabale University |
| issn | 2041-1723 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj-art-50e3de8cd0b549c19e5938b04d6f27602025-02-02T12:32:19ZengNature PortfolioNature Communications2041-17232025-02-0116111310.1038/s41467-024-54721-0Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depressionCyprien A. Rivier0Natalia Szejko1Daniela Renedo2Santiago Clocchiatti-Tuozzo3Shufan Huo4Adam de Havenon5Hongyu Zhao6Thomas M. Gill7Kevin N. Sheth8Guido J. Falcone9Department of Neurology, Yale School of MedicineDepartment of Bioethics, Medical University of WarsawDepartment of Neurology, Yale School of MedicineDepartment of Neurology, Yale School of MedicineDepartment of Neurology, Yale School of MedicineDepartment of Neurology, Yale School of MedicineDepartment of Biostatistics, Yale School of Public HealthDepartment of Internal Medicine, Yale School of MedicineDepartment of Neurology, Yale School of MedicineDepartment of Neurology, Yale School of MedicineAbstract Chronological age is an imperfect estimate of molecular aging. Epigenetic age, derived from DNA methylation data, provides a more nuanced representation of aging-related biological processes. We examine the bidirectional relationship between epigenetic age and brain health events (stroke, dementia, late-life depression) using data from 4,018 participants. Participants with a prior brain health event are 4% epigenetically older (β = 0.04, SE = 0.01), indicating these conditions are associated with accelerated aging beyond that captured by chronological age. Additionally, a one standard deviation increase in epigenetic age is associated with 70% higher odds of experiencing a brain health event in the next four years (OR = 1.70, 95% CI = 1.16–2.50), suggesting epigenetic age acceleration is not just a consequence but also a predictor of poor brain health. Mendelian Randomization analyses replicate these findings, supporting their causal nature. Our results support using epigenetic age as a biomarker to evaluate interventions aimed at preventing and promoting recovery after brain health events.https://doi.org/10.1038/s41467-024-54721-0 |
| spellingShingle | Cyprien A. Rivier Natalia Szejko Daniela Renedo Santiago Clocchiatti-Tuozzo Shufan Huo Adam de Havenon Hongyu Zhao Thomas M. Gill Kevin N. Sheth Guido J. Falcone Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression Nature Communications |
| title | Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression |
| title_full | Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression |
| title_fullStr | Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression |
| title_full_unstemmed | Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression |
| title_short | Bidirectional relationship between epigenetic age and stroke, dementia, and late-life depression |
| title_sort | bidirectional relationship between epigenetic age and stroke dementia and late life depression |
| url | https://doi.org/10.1038/s41467-024-54721-0 |
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