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Review article| Volume 75, P5-10, May 2020

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Neuroinflammation and depressive disorder: The role of the hypothalamus

  • Alena Cernackova
    Correspondence
    Corresponding author at: Institute of Physiology, Faculty of Medicine, Sasinkova 2, 813 72 Bratislava, Slovakia.
    Affiliations
    Institute of Physiology, Faculty of Medicine, Comenius University in Bratislava, Slovakia

    Institute of Experimental Endocrinology, Biomedical Research Center of the Slovak Academy of Sciences, Bratislava, Slovakia
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  • Zdenka Durackova
    Affiliations
    Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University in Bratislava, Slovakia
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  • Jana Trebaticka
    Affiliations
    Department of Child and Adolescent Psychiatry, Faculty of Medicine, Comenius University and Child University Hospital, Bratislava, Slovakia
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  • Boris Mravec
    Affiliations
    Institute of Physiology, Faculty of Medicine, Comenius University in Bratislava, Slovakia

    Institute of Experimental Endocrinology, Biomedical Research Center of the Slovak Academy of Sciences, Bratislava, Slovakia
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Published:March 23, 2020DOI:https://doi.org/10.1016/j.jocn.2020.03.005

      Highlights

      • Hypothalamic inflammation is associated with both somatic and psychiatric diseases.
      • Stress exposure may induce expression of inflammatory molecules in the hypothalamus.
      • Stress, depressive disorder and somatic diseases may be interconnected in hypothalamic inflammation.

      Abstract

      Data accumulated over the last two decades has demonstrated that hypothalamic inflammation plays an important role in the etiopathogenesis of the most prevalent diseases, such as cardiovascular diseases, metabolic syndrome, and even cancer. Recent findings indicate that hypothalamic inflammation is also associated with stress exposure and certain psychiatric diseases, such as depressive disorder. Mechanistic studies have shown that intense and/or chronic stress exposure is accompanied by the synthesis of inflammatory molecules in the hypothalamus, altered hypothalamic–pituitary-adrenal axis activity, and development of glucocorticoid resistance. Consequently, these factors might play a role in the etiopathogenesis of psychiatric disorders. We propose that hypothalamic inflammation represents an interconnection between somatic diseases and depressive disorder. These assumptions are discussed in this mini-review in the light of available data from studies focusing on hypothalamic inflammation.

      Graphical abstract

      Abbreviations:

      ACTH (adrenocorticotropic hormone), ATP (adenosine triphosphate), BDNF (brain derived neutrophic factor), CNS (central nervous system), CRH (corticoliberin), FA (fatty acids), FGF (fibroblast growth factor), GR (glucocorticoid receptor), HPA axis (hypothalamic–pituitary-adrenal axis), Iba1 (calcium-binding adapter molecule 1), ICAM-1 (intracellular cell adhesion molecule 1), IDO (indoleamine 2,3-dioxygenase), IFN-α (interferon α), IL-1β (interleukin 1β), IL-2 (interleukin 2), IL-6 (interleukin 6), IL-10 (interleukin 10), ISC (immune system cells), MAT (metabolically active tissue), NCAM (neural cell adhesion molecule), NF-κB (nuclear factor kappa B), NLRP3 (NOD-like receptor 3), NMDA (N-methyl-D-aspartate), TLRs (toll-like receptors), TNF-α (tumor necrosis factor α), Trp (tryptophan), VCAM-1 (vascular cell adhesion molecule 1), SSRIs (selective serotonin reuptake inhibitors)

      Keywords

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