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Interactions between the apolipoprotein E ε4 allele status and adverse childhood experiences on depressive symptoms in older adults

BACKGROUND: The influence of childhood adversity on depression is modulated by genetic vulnerability. The apolipoprotein E ε4 (APOE-ε4) allele is a strong genetic risk factor for Alzheimer's disease (AD). Because late-life depressive symptoms could be a part of the preclinical course of AD, the...

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Detalles Bibliográficos
Autores principales: Park, Subin, Nam, Yoon-Young, Sim, Yoojin, Hong, Jin Pyo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Co-Action Publishing 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4309830/
https://www.ncbi.nlm.nih.gov/pubmed/25630472
http://dx.doi.org/10.3402/ejpt.v6.25178
Descripción
Sumario:BACKGROUND: The influence of childhood adversity on depression is modulated by genetic vulnerability. The apolipoprotein E ε4 (APOE-ε4) allele is a strong genetic risk factor for Alzheimer's disease (AD). Because late-life depressive symptoms could be a part of the preclinical course of AD, the APOE-ε4 allele may contribute to depression in old age. OBJECTIVE: The aim of this study was to evaluate whether an APOE-ε4 carrier status was associated with depressive symptoms in older adults and to detect the gene–environment interaction between APOE-ε4 status and childhood adversity in relation to depressive symptoms in old age. METHOD: The participants consisted of 137 older adults (age range 50–70) without any psychiatric history or clinically significant cognitive impairment. APOE genotypes and measures of childhood adversity and depressive symptoms were obtained. RESULTS: There was a significant positive association between adverse childhood experiences (ACE) scores and depressive symptoms (B=0.60; 95% CI=0.26, 0.93 for a 1 score increase in ACE scores; p=0.001). Although APOE-ε4 status per se was not associated with depressive symptoms, there was a significant interaction of the ACE scores with the APOE genotype in relation to depressive symptoms (B=0.78; 95% CI=0.02, 1.55; p=0.044). There was a significantly higher effect of childhood adversity on depressive symptoms in APOE-ε4 carriers than non-carriers (t=2.13, p=0.035). CONCLUSIONS: Our results suggest that the APOE-ε4 may modulate the association between childhood adversity and depressive symptoms in older adults. However, more research in a larger sample is needed to gain a better understanding of the relationship between the APOE-ε4, childhood adversity, and depression.