Abstract
Depression is a chronic and prevalent neuropsychiatric disorder; clinical symptoms include excessive sad mood, anhedonia, increased anxiety, disturbed sleep, and cognitive deficits. The exact etiopathogenesis of depression is not well understood. Studies have suggested that tumor necrosis factor-alpha (TNF-alpha) and interleukins (ILs) perform vital roles in the pathogenesis and treatment of depression. Increasing evidence suggests the upregu-lation of TNF-alpha and ILs expression in patients with depression. Therefore, biologics like TNF inhibitors (eta-nercept, infliximab, adalimumab) and IL inhibitors (ustekinumab) have become key compounds in the treatment of depression. Interestingly, treatment with an antidepressant has been found to decrease the TNF-alpha level and improve depression-like behaviors in several preclinical and clinical studies. In the current article, we have reviewed the recent findings linking TNF-alpha and the pathogenesis of depression proving TNF-alpha inhibitors as potential new therapeutic agents. Animal models and clinical studies further support that TNF-alpha inhibitors are effective in ameliorating depression-like behaviors. Moreover, studies showed that peripheral injection of TNF-alpha exhibits depressive symptoms. These symptoms have been improved by treatment with TNF-alpha inhibitors. Hence suggesting TNF-alpha inhibitors as potential new antidepressants for the management of depressive disorder.