Moreover, correlations between IL-6 activity, acute phase proteins, and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis were suggested in severe depression. (1992) established immune cell profile of patients with depression and advocated for the existence of a systemic immune activation during major depressive disorder. However, it is noteworthy that it was probably in the early 1990s that for the first time, possible relationships between the peripheral immune system and major depression was studied. In recent years, “inflammatory hypothesis” has been proposed. Historically, the “monoamine-depletion hypothesis” has been the main proposed pathophysiology nevertheless, this hypothesis alone cannot fully account for pathogenesis of MDD. However, the exact mechanisms underlying inflammation-induced depression are not completely elucidated. Thus, therapeutic deficiency in treatment outcomes reflects the demand for revitalizing psychiatric therapeutics with novel pharmacotherapeutic options that engage non-monoaminergic molecular targets.Ī large body of evidence suggests that inflammation has central role in pathogenesis of MDD. Indeed, there exists no compelling evidence that current treatments are capable of disease modification in MDD patients. Despite available pharmacotherapeutic options, 30–60% of patients with MDD are not responsive to available treatments and the rate of remission of the disease is often < 50%, while recurrence rates are more than 85% within 10 years of a depressive episode, and average about ≥ 50% within 6 months of assumed clinical remission. MDD is characterized by periods of low mood, altered cognition, considerable functional burden including impaired occupational functioning and psychosocial disability. According to worldwide projections, MDD will be the single major cause of burden of all health conditions by 2030. The total estimated number of people living with depression worldwide increased by 49.86% from 1990 to 2017. Major depressive disorder (MDD) is a leading cause of disability throughout the world with a global prevalence of 2.6–5.9%. As IL-6 acts on multiple differing target tissues throughout the body, dysregulation of this particular cytokine can precipitate a multitude of events relevant to depression and blocking its effects can prevent further escalation of inflammatory responses, and potentially pave the way for opening new avenues in diagnosis, treatment, and prevention of this debilitating disorder. Alterations in IL-6 levels, both within the periphery and the brain, most probably contribute to depression symptomatology in numerous ways. Publications between 1980 and July 2020 were included. All peer-reviewed journal articles published before July 2020 for each area discussed were searched by WOS, PubMed, MEDLINE, Scopus, Google Scholar, for original research, review articles, and book chapters. The purpose of the present narrative review was to provide an integrated account of how IL-6 may contribute to development of depression. Recent studies both pre-clinical and clinical have advocated for the functional role of IL-6 in development of MDD and suggested a great potential for targeting this cytokine to open new avenues in pharmacotherapy of depression. Many patients with major depressive disorder (MDD) are reported to have higher levels of multiple inflammatory cytokines including interleukin 6 (IL-6).
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