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Aberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2 antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression.
We recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0–43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest.
Lurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high- v. low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF.
Lurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.
There is little research on children's positive attributes and their
association with psychiatric outcomes.
To examine the hypothesis that children's positive attributes are
associated with a reduced risk of developing psychopathology in
Positive attributes, measured with the Youth Strengths Inventory (YSI)
and psychiatric outcomes were assessed on two occasions over 3 years in a
large epidemiological sample of British children and adolescents
(n = 5325).
The YSI showed high to moderate cross-informant correlations and
longitudinal stability. Children scoring high on positive attributes at
baseline had fewer psychiatric symptoms and disorders at follow-up,
adjusting for symptoms at baseline, disorder at baseline and child and
family factors. Analyses with propensity score matching also suggested
that positive attributes decrease the likelihood of psychiatric
Children's positive attributes are associated with significantly less
psychopathology across time and may be a target for intervention.
Pathways from early-life conduct problems to young adult depression remain poorly understood.
To test developmental pathways from early-life conduct problems to depression at age 18.
Data (n = 3542) came from the Avon Longitudinal Study of Parents and Children (ALSPAC). Previously derived conduct problem trajectories (ages 4–13 years) were used to examine associations with depression from ages 10 to 18 years, and the role of early childhood factors as potential confounders.
Over 43% of young adults with depression in the ALSPAC cohort had a history of child or adolescent conduct problems, yielding a population attributable fraction of 0.15 (95% CI 0.08–0.22). The association between conduct problems and depression at age 18 was considerable even after adjusting for prior depression (odds ratio 1.55, 95% CI 1.24–1.94). Early-onset persistent conduct problems carried the highest risk for later depression. Irritability characterised depression for those with a history of conduct problems.
Early-life conduct problems are robustly associated with later depressive disorder and may be useful targets for early intervention.
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