The Role of PKC Activation in the Immune-inflammatory Mechanism of Major Depressive Depression
Status:
Not yet recruiting
Trial end date:
2024-12-31
Target enrollment:
Participant gender:
Summary
Major Depressive disorder (MDD) is a heterogeneous mental illness. Treated with
antidepressants that act on the neurotransmitter and/or their receptors just remitted only
one third of patients with MDD, Thus, to improve the efficacy is a major unmet need for
depression. Based on the scientific reports, inflammation plays a definite role in the
development and treatment of depression, which may be an important way to understand and
finally solve the problem. Our team found that there were significant changes in tumor
necrosis factor (TNF)-α and other inflammatory factors in depressed patients, which caused
neuronal apoptosis and depressive symptoms; PRKCB1(gene of protein kinase C-β) plays an
anti-inflammatory role by regulating protein kinase C(PKC) activation in specific brain
region, improving neuroplasticity and playing an antidepressant role. In this study, we
assumes that the treatment-resistant depression patients maybe due to the immune inflammation
and PKC activation inconsistency or unsynchronized, which couldn't reversible microglia
polarization and neuronal apoptosis in specific brain regions, then, caused the significant
changes at emotional and cognitive neural circuits, so as to exhibit such as emotional,
cognitive symptoms of depression. Therefore, activating PKC and regulating
immune/inflammatory process will be another way to improve the treatment outcome of
depression. Take consideration, we focus on treatment-resistant depression patients, to
validate the relationship between PKC activation and the immune inflammatory mechanism of
depression, evaluate the antidepressant effect of golimumab or calcium tablet (a PKC
activator) plus escitalopram, and initially proposes idividualized treatment strategies for
MDD.