PKC activation might reduce M1 microglia activation and the release of proinflammatory cytokines such as TNF-α, finally alleviating depressive symptoms in TRD.~Primary objective: This study was designed to address the role of PKC-mediated microglial activation in the clinical outcome of first episode depression.~Secondary objective: To illustrate the impact of PKC-mediated microglial activation on impaired cognition, social function and neuronal plasticity.~The investigators adopted randomized design to test placebo-controlled antidepressant augmentation. Patients were randomized (1:1) into one of the following 2groups: SSRI +golimumab, or SSRI +placebo. The total study duration is 12 weeks
Inflammation that is mediated by microglia activation plays an important role in the pathogenesis of depression. Microglia activation can lead to an increase in the levels of proinflammatory cytokines, including TNF-α, which leads to neuronal apoptosis in the specific neural circuits of some brain regions, abnormal cognition, and treatment-resistant depression (TRD). Protein kinase C (PKC) is a key regulator of the microglia activation process. The investigators assume that the abnormality in PKC might be the serum biomarkers of depression.