The role of neuroinflammation on pathogenesis of affective disorders

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Abstract

Accumulating evidence suggests that neuroinflammation plays an important role in etiology of psychiatric disorders. Neuronflammation involves a combination of psychological, neuroendocrine, and nervous systems resulting in changes of neurotransmitter metabolism, dysregulation of the hypothalamuspituitary-adrenal axis, pathologic microglial cell activation, impaired neuroplasticity, and structural and functional brain changes affecting cognition and emotional behavior. Inflammatory cytokines have been postulated to be the possible link and culprit in the disruption of these systems. The outcome of any type of dysregulation of the immune system in the brain might lead to occurrence of depression, anxiety. This review focuses on the possible impact of dysregulated cytokine networks which may cause pathogenesis of affective disorders such as depression and anxiety.

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The role of inflammation in depression: from evolutionary imperative to modern treatment target.

Andrew Miller, Charles L. Raison (2016)

Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.

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Cytokines and major depression.

Olga Schiepers, Marieke Wichers, Michael Maes (2005)

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.

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Immunological aspects in the neurobiology of suicide: elevated microglial density in schizophrenia and depression is associated with suicide.

Johann Steiner, Hendrik Bielau, Ralf Brisch … (2008)

Suicide has a high prevalence in patients with schizophrenia and affective disorder. Our recent postmortem study [Steiner J, Mawrin C, Ziegeler A, Bielau H, Ullrich O, Bernstein HG, Bogerts B. Distribution of HLA-DR-positive microglia in schizophrenia reflects impaired cerebral lateralization. Acta Neuropathologica (Berl) 2006;112:305-16.] revealed increased microglial densities in two schizophrenic patients who had committed suicide. Therefore, the hypothesis of microglial activation during acute psychosis was proposed. Alternatively, "suicide" could be a diagnosis-independent factor leading to microgliosis. To clarify this question, microglial HLA-DR expression was analyzed by immunohistochemistry in the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), mediodorsal thalamus (MD) and hippocampus of 16 schizophrenics, 14 depressed patients with affective disorder and 10 matched controls. A subgroup of six schizophrenics and seven patients with affective disorder who committed suicide was included. ANOVA revealed no effect of diagnosis on microglial density (DLPFC: P=0.469; ACC: P=0.349; MD: P=0.569; hippocampus: P=0.497). However, significant microgliosis was observed in the DLPFC (P=0.004), ACC (P=0.012) and MD (P=0.004) of suicide patients. A similar trend was seen in the hippocampus (P=0.057). In conclusion, immunological factors may play a hitherto underestimated role in suicide. First, microglial activation might be interpreted as a consequence of presuicidal stress. Second, one might speculate a causal link between microglial activation and suicidal behaviour, such as neuroendocrine factors, cytokines, and nitric oxide, which are released from microglial cells and are known to modulate noradrenergic or serotonergic neurotransmission and thus may trigger suicidality.

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Journal

Journal ID (nlm-ta): J Exerc Rehabil

Journal ID (iso-abbrev): J Exerc Rehabil

Title: Journal of Exercise Rehabilitation

Publisher: Korean Society of Exercise Rehabilitation

ISSN (Print): 2288-176X

ISSN (Electronic): 2288-1778

Publication date Collection: February 2020

Publication date (Electronic): 26 February 2020

Volume: 16

Issue: 1

Pages: 2-9

Affiliations

[1 ]Department of Beauty and Health, Halla University, Wonju, Korea

[2 ]Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea

Author notes

[* ]Corresponding author: Insop Shim, https://orcid.org/0000-0002-8014-9782, Department of Physiology, College of Medicine Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea, E-mail: ishim@ 123456khu.ac.kr

[†]

These authors contributed equally to this study as co-first authors.

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Insop Shim https://orcid.org/0000-0002-8014-9782

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Publisher ID: jer-16-1-2

DOI: 10.12965/jer.2040016.008

PMC ID: 7056473

PubMed ID: 32161729

SO-VID: fc7087c3-bc43-4f7f-9ba6-89193346cbc2

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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

The role of neuroinflammation on pathogenesis of affective disorders

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Most cited references 51

The role of inflammation in depression: from evolutionary imperative to modern treatment target.

Cytokines and major depression.

Immunological aspects in the neurobiology of suicide: elevated microglial density in schizophrenia and depression is associated with suicide.

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