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Background. The role of childhood maltreatment (CM) is believed to be crucial in the aberrant function of reward circuit in adolescent-onset major depressive disorder (AO-MDD). Nevertheless, the impact of abnormalities in the GP-based reward circuit on the association between CM and the severity of AO-MDD remains largely unknown. Methods. The GP-based resting-state functional connectivity (RSFC) was analyzed in a sample of 75 patients with AO-MDD and 80 healthy controls in order to identify potential abnormalities in the GP-based reward circuit in AO-MDD patients. Furthermore, we investigated the possible associations between aberrant GP-based reward circuit functioning, CM and its subtypes (namely, childhood abuse and childhood neglect), and the severity of AO-MDD. Results. Compared to the healthy control group, patients with AO-MDD demonstrated a reduction in RSFC between the left posterior GP and the right dorsomedial prefrontal cortex (DMPFC). Our moderation analysis revealed that the abnormal RSFC between the posterior GP and DMPFC had a moderating effect on the relationship between CM and the severity of AO-MDD. Furthermore, upon further interaction decomposition, we observed a positive correlation between CM and AO-MDD severity exclusively in patients with AO-MDD who exhibited lower RSFC between the posterior GP and DMPFC. For AO-MDD patients with higher RSFC between posterior GP and DMPFC, the relationship between CM and AO-MDD severity was not discernible. Conclusions. Our findings underscore the crucial role of anomalies in the reward circuit in AO-MDD and furnish novel leads for probing the relationship among CM, malfunctioning of the reward circuit, and AO-MDD. [ABSTRACT FROM AUTHOR]

Delayed diagnosis of bipolar disorder (BD) is common. However, diagnostic validity may be enhanced using reliable neurobiological markers for BD. Degree centrality (DC) is one such potential marker that enables researchers to visualize neuronal network abnormalities in the early stages of some neuropsychiatric disorders. In the present study, we measured resting-state DC abnormalities and cognitive deficits in order to identify early neurobiological markers for BD. We recruited 23 patients with BD who had recently experienced manic episodes (duration of illness <2 years) and 46 matched healthy controls. Our findings indicated that patients with BD exhibited DC abnormalities in frontal areas, temporal areas, the right postcentral gyrus, and the posterior lobe of the cerebellum. Moreover, correlation analysis revealed that psychomotor speed indicators were associated with DC in the superior temporal and inferior temporal gyri, while attention indicators were associated with DC in the inferior temporal gyrus, in patients with early BD. Our findings suggest that DC abnormalities in neural emotion regulation circuits are present in patients with early BD, and that correlations between attention/psychomotor speed deficits and temporal DC abnormalities may represent early markers of BD. [ABSTRACT FROM AUTHOR]

Serotonin plays an important role in mood regulation, but the involvement of serotonin pathway genes in the development of bipolar I disorder (BP-I), a mood disorder, is not clear. We selected 21 singlenucleotide polymorphisms (SNPs) within the HTR2A gene, 8 within the SLC6A4 gene and 23 within the TPH2 gene for genotyping using the GoldenGate genotyping assay. A total of 375 patients with BP-I and 475 normal controls were recruited. Two out of 21 SNPs (rs1475196 and rs9567747) in the HTR2A gene and 1/23 SNPs (rs17110566) in the TPH2 gene were significantly associated with BP-I, both genotype-wise and allele-wise. Furthermore, a specific haplotype in the HTR2A gene showed a significant association with BP-I. Our results indicate that the HTR2A and TPH2 genes in the serotonin pathway play important roles in susceptibility to BP-I. [ABSTRACT FROM AUTHOR]