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Our study demonstrated nonlinear modulation of the interaction between COMT and depression on brain function. These findings expand our understanding of the COMT effect underlying the pathophysiology of MDD.

The SRL-coated composite mesh showed minimal formation of intra-abdominal adhesions in a rat model of abdominal wall defect repair.

IntroductionPsychomotor retardation (PMR) in depression is analogous to the hypokinesia in Parkinson's disease, which is associated with the unbalanced direct and indirect pathways of cortico-basal ganglia-thalamo-cortical (CBTC) circuitry. This study hypothesized PMR in major depressive disorder (MDD) should be associated with the hyperactivity of CBTC indirect pathways.ObjectivesTo substantiate the hypothesis that the PMR symptom of MDD might attribute to the hyperactivity of the ortico-basal ganglia-thalamo-cortical indirect pathway which could inhibit psychomotor performance.MethodsWe investigated the intrinsic stiato-subthalamic nucleus (STN)-thalamic functional connectivity (FC), three pivotal hubs of the indirect pathway, in 30 MDD patients with PMR (PMR group) and well matched 30 patients without PMR (NPMR group) at baseline, and 11 patients of each group at follow-up who remitted after antidepressant treatment.ResultsThe results showed increased STN-striatum FC of PMR group at baseline and no more discrepancy at follow-up, and significant correlation between PMR severity and thalamo-STN FC.ConclusionsOur findings suggested the increased STN- striatum FC should be considered as a state biomarker to distinguish MDD patients with PMR from patients without PMR at acute period, and thalamo-STN FC could be identified as the predictor of the PMR severity for MDD patients.Disclosure of interestThe authors have not supplied their declaration of competing interest.