Abstract
Background
The influence of childhood adversity on depression is modulated by genetic vulnerability. The apolipoprotein E ɛ4 (APOE-ɛ4) 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-ɛ4 allele may contribute to depression in old age.
Objective
The aim of this study was to evaluate whether an APOE-ɛ4 carrier status was associated with depressive symptoms in older adults and to detect the gene–environment interaction between APOE-ɛ4 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-ɛ4 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-ɛ4 carriers than non-carriers (t=2.13, p=0.035).
Conclusions
Our results suggest that the APOE-ɛ4 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-ɛ4, childhood adversity, and depression.
For the abstract or full text in other languages, please see Supplementary files under ‘Article Tools’
For the abstract or full text in other languages, please see Supplementary files under ‘Article Tools’
Acknowledgements
This study was supported by the Basic Science Program through the National Research Foundation of Korea (NRF) funded by the Korean government (2013R1A1A3008158).
Notes
For the abstract or full text in other languages, please see Supplementary files under ‘Article Tools’