Abstract
THE DEVELOPMENT OF DEPRESSION AS A DYSFUNCTION OF THE IMMUNE SYSTEM.

*Grishma Patel and Sunita Goswami

ABSTRACT

Major depression is one of the most common neuropsychiatric disorders. The role of inflammation, immune system deregulation and oxidative stress play crucial role in pathophysiology of depression. This review summarises the evidence that chronic low grade inflammation plays an important role in the pathology of depression. Evidence is provided that pro-inflammatory cytokines, together with dysfunctional endocrine and neurotransmitter systems, provide a network of changes that underlie depression. Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is one of the fundamental biological mechanisms that underlie major depression. This hyperactivity is caused by inhibition of glucocorticoid (GC)-induced reduction of HPA axis signaling and increased corticotrophin-releasing hormone (CRH) secretion from the hypothalamic paraventricular nucleus and extra-hypothalamic neurons. Cytokines secreted by both immune and non-immune cells can markedly affect neurotransmission within regulatory brain circuits related to the expression of emotions. Pro- inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) are implicated in the pathophysiology of depression and anxiety disorders. The enzyme indoleamine 2, 3-dioxygenose (IDO) may be an important factor in pathophysiology of depression, it is link between the regulation of immune process and monoaminergic systems. IDO is the rate-limiting enzyme in the kynurenine pathway for tryptophan metabolism and is activated by pro-inflammatory cytokines. Nitric oxide (NO) also participates in signal transduction pathways that result in the release of corticosterone from the adrenal gland. In the central nervous system, prostaglandins (PG) generated by the cyclooxygenase (COX) enzyme are involved in the regulation of HPA axis activity.

Keywords: Stress, Inflammation, Depression.


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