The role of the neuroendocrine and immune systems in the pathogenesis of depression

Abstract

Development of depression is associated with the body's response to prolonged stress, which adversely affects the functioning of the nervous, endocrine and immune systems. Prolonged stress can lead to the development of a so-called allostatic load and reduction of concentration of brain-derived neurotrophic factor. These changes result in impairment of neurogenesis and synaptic remodeling process. This article illustrates the involvement of key mediators of allostasis such as the neuroendocrine and immune systems, in the pathogenesis of depression. The literature concerning the contribution of the neuroendocrine and immune systems to depression incidence was reviewed. Development of depression is associated with disturbance of the body's allostasis and inflammatory activation of the immune system. It leads to a chronic increase in the concentration of cortisol and proinflammatory cytokines, which results in an allostatic load. This load leads to neurodegeneration, eventually causing irreversible cognitive impairment and permanent disability. Determination of the concentration of chemokines and their receptors is an important indicator of activation of the immune and neuroendocrine systems. The activity of these systems reflects the severity of the disease and provides important information for effective antidepressant treatment.

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

“…This model relies on the theory that depression is related to a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and to elevated corticosterone levels resulting from chronic stress (Ogłodek et al, 2014;Zhu et al, 2014;Jacobson, 2014).…”

Duality of Antidepressants and Neuroprotectants

“…This is supported by the results of numerous studies indicating elevated levels of the pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β in plasma of depressed patients (Gold and Irwin 2009; Felger and Lotrich 2013; Toben and Baune 2015). That pro-inflammatory cytokines are directly implicated in MDD has been recently reviewed (Hurley and Tizabi 2013; Anderson and Maes 2014; Müller 2014; Ogłodek et al 2014) and hence will not be discussed in detail here. However, it is of relevance to note that the depression induced by chronic stress may also be due to an increase in the release of pro-inflammatory cytokines (Maes et al 2009; Song and Wang 2011), which in turn can cause a reduction in neurogenesis (Song and Wang 2011; Felger and Lotrich 2013; Ogłodek et al 2014; Stepanichev et al 2014).…”

“…That pro-inflammatory cytokines are directly implicated in MDD has been recently reviewed (Hurley and Tizabi 2013; Anderson and Maes 2014; Müller 2014; Ogłodek et al 2014) and hence will not be discussed in detail here. However, it is of relevance to note that the depression induced by chronic stress may also be due to an increase in the release of pro-inflammatory cytokines (Maes et al 2009; Song and Wang 2011), which in turn can cause a reduction in neurogenesis (Song and Wang 2011; Felger and Lotrich 2013; Ogłodek et al 2014; Stepanichev et al 2014). Indeed, there is a reciprocal interaction between cytokines and neurotrophic factors (Spedding and Gressens 2008).…”

Neuropeptides, Cytokines and Thymus Peptides as Effectors of Interactions Between Thymus and Neuroendocrine System

“…Это указывало на преимущественное проникновение в опухоль мозга клеток Tregs тимического происхожде-ния, что авторы рассматривают как существенный факт в пользу иммунотерапии этого заболевания [59]. Кроме роли в воспалении, повреждении и ответе на бактери-альные инфекции, влияние на мозг процессов, проте-кающих в тимусе, может также проявляться в болезнях поведения и, как отмечалось выше, в ответе на боль [35,60,61]. Тимические пептиды и цитокины могут также определять течение болезни -от защитного действия в острых случаях до предотвращения ее прогрессирования.…”