Peer-reviewed article
Estimating direct and indirect genetic effects on emerging variation in depressive symptoms in early adolescence: a trio polygenic score analysis in the MoBa cohort
Meseret Mamo Bazezew, Bernt Damian Glaser, Laura Hegemann, Adrian Dahl Askelund, Jean‐Baptiste Pingault et al. ·
Summary
Written by AI, not yet AICS's view · claude-sonnet-5-5This study used data from the Norwegian Mother, Father and Child Cohort (MoBa) to examine how a child's own genes and their parents' genes relate to depressive symptoms at ages 8 and 14. It used polygenic scores for major depressive disorder, ADHD, anxiety disorders and educational attainment in within-family models. A child's own genetic liability to depression was linked to depressive symptoms that emerged in early adolescence. Little evidence of parental indirect genetic effects was found, apart from a stable effect of maternal educational attainment scores.
Key points
- Children's own MDD polygenic scores had an adolescence-specific effect on depressive symptoms (β PGS*wave = 0.041, 95% CI 0.017 to 0.065).
- Developmentally-stable direct effects were found for MDD (β = 0.016), ADHD (β = 0.024) and educational attainment (β = -0.02) polygenic scores.
- The only indirect genetic effect found was a stable effect of maternal educational attainment polygenic scores (β = 0.04, 95% CI 0.024 to 0.054).
- Direct genetic effects linked to MDD liability accounted for emerging variation in depressive symptoms in adolescence.
Limitations
The abstract does not describe the sample size, ancestry, or how symptoms were measured. Polygenic score effects are small and the abstract does not cover other influences such as environment. The findings come from a Norwegian cohort and may not apply elsewhere.
Abstract
Abstract Early adolescence is a common period of onset for depressive symptoms. In part, this may reflect a developmental expression of individuals’ genetic propensities as they undergo physiological and hormonal changes and interact with new environments. Many commonly proposed mechanisms assume direct effects of an individual’s own genes on emerging variation in their depressive symptomatology. However, estimates of genetic influence based on analyses in unrelated individuals capture not only direct genetic effects but also genetic effects from parents and other biologically related family members. In data from the Norwegian Mother, Father and Child Cohort (MoBa), we used linear mixed models to distinguish developmentally-stable and adolescence-specific direct and parental indirect genetic effects. In within-family models, we examined effects of polygenic scores for major depressive disorder (MDD), ADHD, anxiety disorders, and educational attainment (EA) on depressive symptoms measured at ages 8 and 14. Children’s own MDD polygenic scores showed adolescence-specific effects on depressive symptoms (β PGS*wave =0.041, [95% CI: 0.017, 0.065]). Developmentally-stable direct effects from children’s polygenic scores for MDD (β = 0.016, [0.006, 0.039]), ADHD (β = 0.024, [0.008, 0.041]) and EA (β=-0.02, [ -0.038, -0.002]) were also evident. The only evidence of indirect genetic effects was a stable effect of maternal EA polygenic scores (β = 0.04, [0.024, 0.054]). Direct genetic effects linked to genetic liability to MDD accounted for emerging variation in depressive symptoms in adolescence. These results imply that specific etiological mechanisms related to MDD may become particularly relevant for depressive symptoms during early adolescence compared to at earlier ages.