Cited 51 times in
A DNA methylation clock associated with age-related illnesses and mortality is accelerated in men with combat PTSD
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 강지인 | - |
dc.date.accessioned | 2022-05-09T16:51:03Z | - |
dc.date.available | 2022-05-09T16:51:03Z | - |
dc.date.issued | 2021-09 | - |
dc.identifier.issn | 1359-4184 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/188241 | - |
dc.description.abstract | DNA methylation patterns at specific cytosine-phosphate-guanine (CpG) sites predictably change with age and can be used to derive "epigenetic age", an indicator of biological age, as opposed to merely chronological age. A relatively new estimator, called "DNAm GrimAge", is notable for its superior predictive ability in older populations regarding numerous age-related metrics like time-to-death, time-to-coronary heart disease, and time-to-cancer. PTSD is associated with premature mortality and frequently has comorbid physical illnesses suggestive of accelerated biological aging. This is the first study to assess DNAm GrimAge in PTSD patients. We investigated the acceleration of GrimAge relative to chronological age, denoted "AgeAccelGrim" in combat trauma-exposed male veterans with and without PTSD using cross-sectional and longitudinal data from two independent well-characterized veteran cohorts. In both cohorts, AgeAccelGrim was significantly higher in the PTSD group compared to the control group (N = 162, 1.26 vs -0.57, p = 0.001 and N = 53, 0.93 vs -1.60 Years, p = 0.008), suggesting accelerated biological aging in both cohorts with PTSD. In 3-year follow-up study of individuals initially diagnosed with PTSD (N = 26), changes in PTSD symptom severity were correlated with AgeAccelGrim changes (r = 0.39, p = 0.049). In addition, the loss of CD28 cell surface markers on CD8 + T cells, an indicator of T-cell senescence/exhaustion that is associated with biological aging, was positively correlated with AgeAccelGrim, suggesting an immunological contribution to the accelerated biological aging. Overall, our findings delineate cellular correlates of biological aging in combat-related PTSD, which may help explain the increased medical morbidity and mortality seen in this disease. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Nature Publishing Group Specialist Journals | - |
dc.relation.isPartOf | MOLECULAR PSYCHIATRY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Aged | - |
dc.subject.MESH | Aging / genetics | - |
dc.subject.MESH | Cross-Sectional Studies | - |
dc.subject.MESH | DNA Methylation* / genetics | - |
dc.subject.MESH | Epigenesis, Genetic | - |
dc.subject.MESH | Epigenomics | - |
dc.subject.MESH | Follow-Up Studies | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Stress Disorders, Post-Traumatic* / genetics | - |
dc.title | A DNA methylation clock associated with age-related illnesses and mortality is accelerated in men with combat PTSD | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Psychiatry (정신과학교실) | - |
dc.contributor.googleauthor | Ruoting Yang | - |
dc.contributor.googleauthor | Gwyneth W Y Wu | - |
dc.contributor.googleauthor | Josine E Verhoeven | - |
dc.contributor.googleauthor | Aarti Gautam | - |
dc.contributor.googleauthor | Victor I Reus | - |
dc.contributor.googleauthor | Jee In Kang | - |
dc.contributor.googleauthor | Janine D Flory | - |
dc.contributor.googleauthor | Duna Abu-Amara | - |
dc.contributor.googleauthor | PTSD Systems Biology Consortium | - |
dc.contributor.googleauthor | Leroy Hood | - |
dc.contributor.googleauthor | Francis J Doyle 3rd | - |
dc.contributor.googleauthor | Rachel Yehuda | - |
dc.contributor.googleauthor | Charles R Marmar | - |
dc.contributor.googleauthor | Marti Jett | - |
dc.contributor.googleauthor | Rasha Hammamieh | - |
dc.contributor.googleauthor | Synthia H Mellon | - |
dc.contributor.googleauthor | Owen M Wolkowitz | - |
dc.identifier.doi | 10.1038/s41380-020-0755-z | - |
dc.contributor.localId | A00084 | - |
dc.relation.journalcode | J02269 | - |
dc.identifier.eissn | 1476-5578 | - |
dc.identifier.pmid | 32382136 | - |
dc.identifier.url | https://www.nature.com/articles/s41380-020-0755-z | - |
dc.contributor.alternativeName | Kang, Jee In | - |
dc.contributor.affiliatedAuthor | 강지인 | - |
dc.citation.volume | 26 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 4999 | - |
dc.citation.endPage | 5009 | - |
dc.identifier.bibliographicCitation | MOLECULAR PSYCHIATRY, Vol.26(9) : 4999-5009, 2021-09 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.