Authors : Nitu; Dr. Arun Garg; S. Gopika; Dr. Ashutosh Upadhayay; Dr. Yogender Singh; Badal Tanwar; Chetna

Volume/Issue : Volume 11 - 2026, Issue 5 - May

Google Scholar : https://tinyurl.com/44z94fmz

Scribd : https://tinyurl.com/5cczvkaj

DOI : https://doi.org/10.38124/ijisrt/26May354

Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.

Abstract : Introduction: Depression is a multifactorial psychiatric disorder closely associated with chronic inflammation and stress. The nuclear factor kappa-B (NF-κB) signalling pathway, a major regulator of immune and inflammatory responses, has emerged as a key molecular link between these factors and depression. Under chronic stress, NF-κB becomes over activated in neurons and glial cells, promoting the release of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. This heightened inflammatory response contributes to oxidative stress, neuronal dysfunction, and reduced neuroplasticity—central features of depressive disorders.  Methods: This study employed a comprehensive literature review approach to investigate the role of the NF-κB signaling pathway in the pathophysiology of depression. The search used keywords such as “NF-κB,” “depression,” “inflammation,” “cytokines,” and “BDNF.” Both experimental (animal and cellular) and clinical studies were included to evaluate molecular mechanisms linking NF-κB activation with depressive symptoms.  Results: This review shows that NF-κB overactivation increases cytokines and oxidative stress, causing neuronal dysfunction. The Notch2/NF-κB pathway increases stress susceptibility, while NF-κB inhibition reduces depressive behaviours, suggesting therapeutic potential.  Conclusion: NF-κB overactivation links inflammation and depression by impairing neuroplasticity and hormonal balance. Targeting this pathway may help reduce neuroinflammation and improve depressive symptoms. Further research should explore NF-κB inhibitors in clinical settings.

Keywords : NF-κB, Depression, Inflammation, BDNF, Cytokines.

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