Major depressive esq watch repair disorder (MDD) is a clinical syndrome defined by chronic disturban

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The electronic version of this article is the complete one and can be found online at: http://www.jneuroinflammation.com/content/11/1/11 Received: 5 December 2013 Accepted: 7 January esq watch repair 2014 Published: 21 January 2014
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Although major depressive disorder imposes a serious public health esq watch repair burden and affects esq watch repair nearly one in six individuals in developed countries over their lifetimes, there is still no consensus on its pathophysiology. Inflammation and cytokines have emerged as a promising new avenue in depression research, and, in particular, macrophage migration inhibitory factor (MIF) has been shown to be significant in depression physiology. In this review we summarize current research on MIF and depression. We highlight the arguments for MIF as a pro- and antidepressant species and discuss the potential implications for therapeutics. Keywords: MIF; Depression; Neuroinflammation; Neurogenesis; Antidepressant; Biomarker Introduction
Major depressive esq watch repair disorder (MDD) is a clinical syndrome defined by chronic disturbances in emotion and ideation that are accompanied by somatic or neurovegetative symptoms [ 1 ]. The disease has a worldwide lifetime prevalence of 12%, with the prevalence in developed countries (USA and Europe) as high as 18% [ 2 ]; this figure is increasing over time [ 3 ]. Additionally, depressive mood is often comorbid with other psychiatric conditions such as anxiety and eating disorders, as well as with chronic esq watch repair medical conditions such as cancer, cardiovascular disease, neurological disorders, esq watch repair and chronic inflammatory diseases [ 4 ]; this is often called secondary depression [ 5 ]. Comorbid depression significantly esq watch repair worsens outcomes in coronary heart disease, diabetes mellitus, and stroke [ 6 , 7 ]. Depression can also cause cognitive symptoms [ 8 ] that can produce severe psychosocial deficits [ 9 ]. Despite these considerations, treatment for depression has not changed significantly in recent years. Current treatments esq watch repair do not adequately address cognitive deficits in depression [ 10 ], and there remain few solutions for treatment-resistant depression, which affects almost half of the patient population [ 11 ].
One of the reasons for the slow progress in this area is the lack of a unified theory of the pathobiology of depression. Several hypotheses are currently supported esq watch repair by research. One of the oldest is the monoamine theory, which asserts that depression is caused by a depletion of monoamines (such as serotonin or norepinephrine) in the brain [ 12 ]. Selective serotonin reuptake inhibitors (SSRIs) operate on this premise, and they are currently among the first-line treatments esq watch repair for major depression [ 13 ]. However, this theory fails to explain the delay in remission during treatment with SSRIs, or why depletion of monoamines does not reproduce depressive symptoms in healthy controls. As a result, a neurotrophic theory of depression has emerged: atrophic changes are found in the postmortem brains of MDD patients, and increases in neurogenesis or neuroplastic factors have antidepressant effects [ 12 ]. Any unified theory of depression would doubtless need to incorporate aspects of both of these hypotheses.
A large body of evidence has also pointed to an inflammatory etiology in depression [ 14 ]. Depressed mood develops in nearly a third of patients treated with recombinant interferon alpha, and is more prevalent in patients with chronic inflammatory diseases [ 15 , 16 ]. Systemic inflammation produces sickness behavior esq watch repair that resembles depression in both patients and rodent models [ 17 ]. One of the challenges of this hypothesis is explaining how peripheral cytokines can cross the blood brain barrier and affect the central nervous system to induce depression. One proposed explanation centers on the cytokine-activated enzyme indoleamine 2,3-dioxygenase, which has been shown to induce depression-like behavior. It degrades neural tryptophan into 3-hydroxykyurenin and quinolinic acid; in addition to being neurotoxic, these metabolites also drain local stores of tryptophan, which is a prerequisite in the synthesis of ser