B-94: Examining the Relationship Between Psychosocial Stressors, Neuroinflammation, Neuroplasticity, and the Pathology of Depression
Abstract
Objective: This review examines how psychosocial stressors influence microglial activity and contribute to neuroinflammation that could potentially impair adaptive neuroplasticity in depression. Depression is increasingly understood as a disorder involving neuroimmune dysfunction, with neuroinflammation playing a central role in its pathophysiology. Psychosocial stressors have been shown to influence immune signaling in the brain, particularly through microglial activation. The mechanisms linking these stressors to impaired adaptive neuroplasticity, as well as the barriers they create for effective treatment, remain insufficiently integrated in the literature. Method/Data Selection: A systematic literature search was conducted in databases such as PubMed and PsycINFO to identify studies examining microglial activation, neuroinflammation, and neuroplasticity in depression. Emphasis was placed on the pathways linking stress exposure to microglial-mediated changes in brain function and structure. Results/Data Synthesis: Studies consistently demonstrate a correlation between chronic psychosocial stressors, increased microglial activity, neuroinflammation, and neuroplasticity. Neuroplastic changes were consistently noted in the following brain regions: hippocampus, grey matter, prefrontal cortex, anterior cingulate cortex, and amygdala. Common findings related to neuroplastic changes included decreased structural volume in specific brain regions associated with mood, emotions, and behavior; increased microglial activity; decreased neurogenesis; and dysregulation of neuronal communication pathways. Conclusions: While current research indicates a bidirectional relationship between psychosocial stressors, increased microglial activity, neuroinflammation, neuroplasticity, and the pathology of depression, the specific mechanisms leading to change are not fully understood. Future research should focus on examining the indicated brain regions and associated mechanisms that lead to impairment in adaptive neuroplasticity, while also identifying accessible and applicable interventions to support adaptive neuroplasticity as a means of treatment.