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Maternal mental health strongly influences child development and depression risk. This study investigated how positive and negative dimensions of prenatal maternal mental health differentially shape childhood depressive symptoms through cognitive mediators.
Methods
Participants were drawn from the Growing Up in Singapore Towards Healthy Outcomes (GUSTO) cohort. Of the 1198 mother–child dyads enrolled, 523 (52.6% boys) had sufficient data for the mediation analysis. Maternal mental health at 26 weeks’ gestation was assessed using a bifactor model derived from the Beck Depression Inventory-II, State–Trait Anxiety Inventory, and Edinburgh Postnatal Depression Scale. Child language ability was measured at age 2 years with the Bayley Scales of Infant Development, executive function at age 7 years with the Behaviour Rating Inventory of Executive Function, and depressive symptoms at age 9 years with the Children’s Depression Inventory-2. Serial mediation models tested hypothesized pathways.
Results
Distinct mediation pathways emerged. Positive maternal mental health was associated with enhanced early language ability, which in turn was associated with fewer depressive symptoms in later childhood (β = −0.017, 95% CI: −0.042, −0.003). Conversely, negative maternal mental health was associated with poorer executive functioning, which in turn was associated with more depressive symptoms (β = 0.040, 95% CI: 0.016–0.077).
Conclusions
Positive and negative maternal mental health are linked to childhood depressive symptoms through distinct neurocognitive pathways. By identifying language and executive function as specific developmental mediators, our findings point to targeted and developmentally sensitive intervention opportunities to disrupt intergenerational pathways of depression.
Screen time in infancy is linked to changes in social-emotional development but the pathway underlying this association remains unknown. We aim to provide mechanistic insights into this association using brain network topology and to examine the potential role of parent–child reading in mitigating the effects of screen time.
Methods
We examined the association of screen time on brain network topology using linear regression analysis and tested if the network topology mediated the association between screen time and later socio-emotional competence. Lastly, we tested if parent–child reading time was a moderator of the link between screen time and brain network topology.
Results
Infant screen time was significantly associated with the emotion processing-cognitive control network integration (p = 0.005). This network integration also significantly mediated the association between screen time and both measures of socio-emotional competence (BRIEF-2 Emotion Regulation Index, p = 0.04; SEARS total score, p = 0.04). Parent–child reading time significantly moderated the association between screen time and emotion processing-cognitive control network integration (β = −0.640, p = 0.005).
Conclusion
Our study identified emotion processing-cognitive control network integration as a plausible biological pathway linking screen time in infancy and later socio-emotional competence. We also provided novel evidence for the role of parent–child reading in moderating the association between screen time and topological brain restructuring in early childhood.
Earlier studies examining structural brain abnormalities associated with cognitively derived subgroups were mainly cross-sectional in design and had mixed findings. Thus, we obtained cross-sectional and longitudinal data to characterize the extent and trajectory of brain structure abnormalities underlying distinct cognitive subtypes (“preserved,” “deteriorated,” and “compromised”) seen in psychotic spectrum disorders.
Methods.
Data from 364 subjects (225 patients with psychotic conditions and 139 healthy controls) were first used to determine the relationship of cognitive subtypes with cross-sectional measures of subcortical volume and cortical thickness. To probe neurodevelopmental abnormalities, brain structure laterality was examined. To examine whether neuroprogressive abnormalities persist, longitudinal brain structural changes over 5 years were examined within a subset of 101 subjects. Subsequent discriminant analysis using the identified brain measures was performed on an independent subject group.
Results.
Cross-sectional comparisons showed that cortical thinning and limbic volume reductions were most widespread in “deteriorated” cognitive subtype. Laterality comparisons showed more rightward amygdala lateralization in “compromised” than “preserved” subtype. Longitudinal comparisons revealed progressive hippocampal shrinkage in “deteriorated” compared with healthy controls and “preserved” subtype, which correlated with worse negative symptoms, cognitive and psychosocial functioning. Post-hoc discrimination analysis on an independent group of 52 subjects using the identified brain structures found an overall accuracy of 71% for classification of cognitive subtypes.
Conclusion.
These findings point toward distinct extent and trajectory of corticolimbic abnormalities associated with cognitive subtypes in psychosis, which can allow further understanding of the biological course of cognitive functioning over illness course and with treatment.
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