Glucocorticoid receptor gene (NR3C1) methylation, childhood maltreatment, multilevel reward responsiveness and depressive and anxiety symptoms: A neuroimaging epigenetic study
Background: Although epigenomic and environment interactions (Epigenome × Environment; Epi × E) might constitute a novel mechanism underlying reward processing, direct evidence is still scarce. We conducted the first longitudinal study to investigate the extent to which DNA methylation of a stress-r...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-02-01
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| Series: | NeuroImage |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1053811925000035 |
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| Summary: | Background: Although epigenomic and environment interactions (Epigenome × Environment; Epi × E) might constitute a novel mechanism underlying reward processing, direct evidence is still scarce. We conducted the first longitudinal study to investigate the extent to which DNA methylation of a stress-related gene—NR3C1—interacts with childhood maltreatment in association with young adult reward responsiveness (RR) and the downstream risk of depressive (anhedonia dimension in particular) and anxiety symptoms. Method: A total of 192 Chinese university students aged 18∼25 (Mage = 21.08 ± 1.91 years; 59.4% females) were followed in two waves. Reward positivity (RewP) and its time‒frequency components were elicited via a classic monetary reward task. Cytosine methylation in the promoter exon 1F of NR3C1 (NR3C1-1F) was sequenced via buccal cells. Childhood maltreatment, self-reported RR and depressive and anxiety symptoms were assessed via questionnaires. Results: NR3C1-1F methylation significantly interacted with childhood maltreatment on RewP but not the delta and theta components or self-reported RR. The severity and exposure number of childhood maltreatment were negatively associated with RewP among individuals with heightened NR3C1-1F methylation but positively associated with RewP among individuals with blunted NR3C1-1F methylation, demonstrating a “goodness-of-fit” interaction. This interaction was specifically linked with anhedonia dimension but not with total scores of depressive or anxiety symptoms. Conclusions: The current findings provide preliminary evidence for an Epi × E interaction underlying reward processing, highlight cross-level analyses of electrophysiological signals and advance knowledge of the biological foundation of stress-induced reward function and relevant symptoms. However, caution should be paid to the generalizability of these findings in high-risk clinical samples given the high-functioning characteristic of the present sample. |
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| ISSN: | 1095-9572 |