Major depressive disorder (MDD) is a leading cause of global disability and is associated with substantial functional impairment, medical comorbidity, and premature mortality.Despite significant advances in antidepressant pharmacotherapy, approximately one-third of patients fail to achieve an adequate response to first-line treatment, underscoring the biological heterogeneity of the disorder.Growing evidence implicates immune-inflammatory dysregulation and impaired neuroplasticity as central mechanisms underlying vulnerability to depression, symptom heterogeneity, illness chronicity, and treatment resistance.Elevated inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-2 (IL-2), and tumor necrosis factor- (TNF-), and reduced levels of brain-derived neurotrophic factor (BDNF) have been consistently associated with depressive symptom severity, cognitive impairment, recurrent illness, and poor treatment outcomes.This review synthesizes current evidence on the role of inflammatory and neurotrophic markers in the etiology of MDD, their association with clinical features and the course of illness, and their implications for antidepressant response and personalized treatment approaches.
Jeenger et al. (Tue,) studied this question.