Journal ArticleDOI
Cytokines and major depression.
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TLDR
Although the central effects of proinflammatory cytokines appear to be able to account for most of the symptoms occurring in depression, it remains to be established whether cytokines play a causal role in depressive illness or represent epiphenomena without major significance.Abstract:
In the research field of psychoneuroimmunology, accumulating evidence has indicated the existence of reciprocal communication pathways between nervous, endocrine and immune systems. In this respect, there has been increasing interest in the putative involvement of the immune system in psychiatric disorders. In the present review, the role of proinflammatory cytokines, such as interleukin (IL)-1, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma, in the aetiology and pathophysiology of major depression, is discussed. The 'cytokine hypothesis of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioural, neuroendocrine and neurochemical features of depressive disorders. This view is supported by various findings. Several medical illnesses, which are characterised by chronic inflammatory responses, e.g. rheumatoid arthritis, have been reported to be accompanied by depression. In addition, administration of proinflammatory cytokines, e.g. in cancer or hepatitis C therapies, has been found to induce depressive symptomatology. Administration of proinflammatory cytokines in animals induces 'sickness behaviour', which is a pattern of behavioural alterations that is very similar to the behavioural symptoms of depression in humans. The central action of cytokines may also account for the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity that is frequently observed in depressive disorders, as proinflammatory cytokines may cause HPA axis hyperactivity by disturbing the negative feedback inhibition of circulating corticosteroids (CSs) on the HPA axis. Concerning the deficiency in serotonergic (5-HT) neurotransmission that is concomitant with major depression, cytokines may reduce 5-HT levels by lowering the availability of its precursor tryptophan (TRP) through activation of the TRP-metabolising enzyme indoleamine-2,3-dioxygenase (IDO). Although the central effects of proinflammatory cytokines appear to be able to account for most of the symptoms occurring in depression, it remains to be established whether cytokines play a causal role in depressive illness or represent epiphenomena without major significance.read more
Citations
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Anxiolytic- and antidepressant-like effects of Silymarin compared to diazepam and fluoxetine in a mouse model of mild traumatic brain injury.
Morteza Kosari-Nasab,Ghaffar Shokouhi,Amir Ghorbanihaghjo,Mehran Mesgari Abbasi,Ali-Akbar Salari +4 more
TL;DR: The results showed that DZP, FLX or SIL can significantly reduce anxiety‐ and depression‐like symptoms, and neuroinflammation after mTBI induction in mice, and these drugs reduced TNF‐&agr; levels in the prefrontal cortex and hippocampus.
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The Kynurenine Pathway in the Acute and Chronic Phases of Cerebral Ischemia.
María Isabel Cuartero,Juan de la Parra,Alicia García-Culebras,Iván Ballesteros,Ignacio Lizasoain,María A. Moro +5 more
TL;DR: The KP contribution in the ischemic damage, how the unbalance of the KP might trigger an alteration of the cognitive function after stroke as well as potential targets for the development of new drugs are detailed.
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Dietary interventions with n-3 fatty acids or probiotics targeting post-myocardial infarction depression.
TL;DR: It is demonstrated that a diet containing either high n-3 PUFA or probiotics, when given after the onset of ischaemia/reperfusion, is also able to inhibit apoptosis in the limbic system, reduce circulating levels of pro-inflammatory cytokines and attenuate post-MI depression.
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The dose makes the poison: from glutamate-mediated neurogenesis to neuronal atrophy and depression.
TL;DR: Data suggest that the glutamatergic system could be a final common pathway for antidepressant treatments, and various studies show that treatment with antidepressants decreases plasma glutamate levels in depressed individuals and regulates glutamate receptors.
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Pathophysiological mechanisms involved in the relationship between diabetes and major depressive disorder
Gislaine Z. Réus,Maria Augusta B Dos Santos,Ana Paula Strassi,Helena M. Abelaira,Luciane Bisognin Ceretta,João Quevedo +5 more
TL;DR: This study reviewed the literature relating to the relationship between MDD and DM, bringing forward studies showing that DM develops due to MDD, and others that report the opposite.
References
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Book
Immunobiology: The Immune System in Health and Disease
TL;DR: Introductory immunology textbook for medical students, advanced undergraduates, and graduate students.
Journal ArticleDOI
The inflammatory reflex
TL;DR: The discovery that cholinergic neurons inhibit acute inflammation has qualitatively expanded understanding of how the nervous system modulates immune responses, and the opportunity now exists to apply this insight to the treatment of inflammation through selective and reversible 'hard-wired' neural systems.
Journal ArticleDOI
The catecholamine hypothesis of affective disorders: a review of supporting evidence
TL;DR: The "catecholamine hypothesis of affective disorders" as discussed by the authors suggests that depression is associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites.
Journal ArticleDOI
A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate.
Michael E. Weinblatt,Joel M. Kremer,Arthur D. Bankhurst,Ken J. Bulpitt,Roy Fleischmann,Robert I. Fox,Christopher G. Jackson,Mary Lange,Daniel Burge +8 more
TL;DR: In patients with persistently active rheumatoid arthritis, the combination of etanercept and methotrexate was safe and well tolerated and provided significantly greater clinical benefit than metotrexate alone.