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Neuroinflammation and depression: A review.

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Title: Neuroinflammation and depression: A review.
Authors: Troubat, Romain (AUTHOR), Barone, Pascal (AUTHOR), Leman, Samuel (AUTHOR), Desmidt, Thomas (AUTHOR), Cressant, Arnaud (AUTHOR), Atanasova, Boriana (AUTHOR), Brizard, Bruno (AUTHOR), El Hage, Wissam (AUTHOR), Surget, Alexandre (AUTHOR), Belzung, Catherine (AUTHOR), Camus, Vincent (AUTHOR)
Source: European Journal of Neuroscience. Jan2021, Vol. 53 Issue 1, p151-171. 21p. 1 Diagram, 2 Charts.
Subjects: Inflammation, Mental depression, Dentate gyrus, Blood-brain barrier, Psychoneuroimmunology, Neurodegeneration, Dysthymic disorder
Abstract: Some recent clinical and preclinical evidence suggests that neuroinflammation is a key factor that interacts with the three neurobiological correlates of major depressive disorder: depletion of brain serotonin, dysregulation of the hypothalamus–pituitary–adrenal (HPA) axis and alteration of the continuous production of adult‐generated neurons in the dentate gyrus of the hippocampus. This review discusses the main players in brain immunity as well as how inflammation interacts with the above three mechanisms. It is reported that kynurenine (KYN) pathway alteration in favour of its excitotoxic component and HPA axis dysregulation have the common effect of increasing extracellular glutamate levels and glutamate neurotransmission, which can impact hippocampal neurogenesis. This pathophysiological cascade appears to be triggered or sustained and reinforced by any chronic inflammatory condition involving increased circulating markers of inflammation that are able to cross the blood–brain barrier and activate microglia; it can also be the consequence of primary brain neuroinflammation, such as in neurodegenerative disorders with early manifestations that are frequently depressive symptoms. Further recent data indicate that primary microglial activation may also result from a direct impact of chronic stress on vascular function. The intricated dynamic crosstalk between neuroinflammation and other relevant neurobiological correlates of depression add to evidence that neuroinflammation may be a key therapeutic target for future therapeutic strategies in major depressive disorder. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Neuroinflammation and depression: A review.
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  Data: <searchLink fieldCode="AR" term="%22Troubat%2C+Romain%22">Troubat, Romain</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Barone%2C+Pascal%22">Barone, Pascal</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Leman%2C+Samuel%22">Leman, Samuel</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Desmidt%2C+Thomas%22">Desmidt, Thomas</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Cressant%2C+Arnaud%22">Cressant, Arnaud</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Atanasova%2C+Boriana%22">Atanasova, Boriana</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Brizard%2C+Bruno%22">Brizard, Bruno</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22El+Hage%2C+Wissam%22">El Hage, Wissam</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Surget%2C+Alexandre%22">Surget, Alexandre</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Belzung%2C+Catherine%22">Belzung, Catherine</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Camus%2C+Vincent%22">Camus, Vincent</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Jan2021, Vol. 53 Issue 1, p151-171. 21p. 1 Diagram, 2 Charts.
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  Data: <searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink><br /><searchLink fieldCode="DE" term="%22Mental+depression%22">Mental depression</searchLink><br /><searchLink fieldCode="DE" term="%22Dentate+gyrus%22">Dentate gyrus</searchLink><br /><searchLink fieldCode="DE" term="%22Blood-brain+barrier%22">Blood-brain barrier</searchLink><br /><searchLink fieldCode="DE" term="%22Psychoneuroimmunology%22">Psychoneuroimmunology</searchLink><br /><searchLink fieldCode="DE" term="%22Neurodegeneration%22">Neurodegeneration</searchLink><br /><searchLink fieldCode="DE" term="%22Dysthymic+disorder%22">Dysthymic disorder</searchLink>
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  Label: Abstract
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  Data: Some recent clinical and preclinical evidence suggests that neuroinflammation is a key factor that interacts with the three neurobiological correlates of major depressive disorder: depletion of brain serotonin, dysregulation of the hypothalamus–pituitary–adrenal (HPA) axis and alteration of the continuous production of adult‐generated neurons in the dentate gyrus of the hippocampus. This review discusses the main players in brain immunity as well as how inflammation interacts with the above three mechanisms. It is reported that kynurenine (KYN) pathway alteration in favour of its excitotoxic component and HPA axis dysregulation have the common effect of increasing extracellular glutamate levels and glutamate neurotransmission, which can impact hippocampal neurogenesis. This pathophysiological cascade appears to be triggered or sustained and reinforced by any chronic inflammatory condition involving increased circulating markers of inflammation that are able to cross the blood–brain barrier and activate microglia; it can also be the consequence of primary brain neuroinflammation, such as in neurodegenerative disorders with early manifestations that are frequently depressive symptoms. Further recent data indicate that primary microglial activation may also result from a direct impact of chronic stress on vascular function. The intricated dynamic crosstalk between neuroinflammation and other relevant neurobiological correlates of depression add to evidence that neuroinflammation may be a key therapeutic target for future therapeutic strategies in major depressive disorder. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/ejn.14720
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        Text: English
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      – SubjectFull: Inflammation
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      – SubjectFull: Dentate gyrus
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      – SubjectFull: Dysthymic disorder
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              Text: Jan2021
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