Epigenetic Aging Associations With Psychoneurological Symptoms and Social Functioning in Adults With Sickle Cell Disease.

Autor:	Knisely MR; Duke University School of Nursing, Durham, NC, USA., Masese RV; Center for Bioethics, Department of Social Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA., Mathias JG; Division of Women's Community and Population Health, Department of Obstetrics and Gynecology, Duke University School of Medicine, Durham, NC, USA., Yang Q; Duke University School of Nursing, Durham, NC, USA., Hatch D; Duke University School of Nursing, Durham, NC, USA., Lê BM; Duke Molecular Physiology Institute, Durham, NC, USA., Luyster F; University of Pittsburgh School of Nursing, Pittsburgh, PA, USA., Garrett ME; Duke Molecular Physiology Institute, Durham, NC, USA., Tanabe PJ; Duke University School of Nursing, Durham, NC, USA., Shah NR; Department of Medicine, Duke University School of Medicine, Durham, NC, USA., Ashley-Koch A; Duke Molecular Physiology Institute and Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
Jazyk:	angličtina
Zdroj:	Biological research for nursing [Biol Res Nurs] 2024 Oct; Vol. 26 (4), pp. 508-517. Date of Electronic Publication: 2024 Apr 28.
DOI:	10.1177/10998004241250322
Abstrakt:	Objective: Sickle cell disease (SCD), the most common inherited blood disorder in the United States, is associated with severe psychoneurological symptoms. While epigenetic age acceleration has been linked to psychoneurological symptom burden in other diseases, this connection is unexplored in SCD. This study aimed to assess the association between epigenetic age acceleration and psychoneurological symptom burden in SCD. Methods: In this cross-sectional study, emotional impact, pain impact, sleep impact, social functioning, and cognitive function were assessed in 87 adults living with SCD. DNA methylation data were generated from blood specimens and used to calculate epigenetic age using five clocks (Horvath, Hannum, PhenoAge, GrimAge, & DunedinPACE). Associations between epigenetic age acceleration and symptoms were assessed. Results: The sample ( N = 87) had a mean (SD) chronologic age was 30.6 (8.1) years. Epigenetic age acceleration was associated with several symptom outcomes. GrimAge age acceleration (β = -0.49, p = .03) and increased DunedinPACE (β = -2.23, p = .004) were associated with worse emotional impact scores. PhenoAge (β = -0.32, p = .04) and the GrimAge (β = -0.48, p = .05) age acceleration were associated with worse pain impact scores. Increased DunedinPACE (β = -2.07 p = .04) were associated with worse sleep impact scores. Increased DunedinPACE (β = -2.87, p = .005) was associated with worse social functioning scores. We did not find associations between epigenetic age acceleration and cognitive function in this sample. Conclusion: Epigenetic age acceleration was associated with worse symptom experiences, suggesting the potential for epigenetic age acceleration as a biomarker to aid in risk stratification or targets for intervention to mitigate symptom burden in SCD. Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Databáze:	MEDLINE
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