COVID-19, Oxidative Stress, and Neuroinflammation in the Depression Route

J Mol Neurosci. 2022 Jun;72(6):1166-1181. doi: 10.1007/s12031-022-02004-y. Epub 2022 Mar 23.

Abstract

COVID-19 is associated with oxidative stress, peripheral hyper inflammation, and neuroinflammation, especially in individuals with a more severe form of the disease. Some studies provide evidence on the onset or exacerbation of major depressive disorder (MDD), among other psychiatric disorders due to COVID-19. Oxidative stress and neuroinflammation are associated conditions, especially in the more severe form of MDD and in refractoriness to available therapeutic strategies. Inflammatory cytokines in the COVID-19 hyper inflammation process can activate the hypothalamic-pituitary-adrenal (HPA) axis and the indoleamine-2,3-dioxygenase (IDO) enzyme. IDO activation can reduce tryptophan and increase toxic metabolites of the kynurenine pathway, which increases glial activation, neuroinflammation, toxicity, and neuronal death. This review surveyed a number of studies and analyzed the mechanisms of oxidative stress, inflammation, and neuroinflammation involved in COVID-19 and depression. Finally, the importance of more protocols that can help elucidate the interaction between these mechanisms underlying COVID-19 and MDD and the possible therapeutic strategies involved in the interaction of these mechanisms are highlighted.

Keywords: COVID-19; Glial activation; Major depressive disorder; Neuroinflammation; Oxidative stress.

Publication types

  • Review

MeSH terms

  • COVID-19*
  • Depression
  • Depressive Disorder, Major* / drug therapy
  • Humans
  • Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism
  • Inflammation
  • Kynurenine / metabolism
  • Kynurenine / therapeutic use
  • Neuroinflammatory Diseases
  • Oxidative Stress

Substances

  • Indoleamine-Pyrrole 2,3,-Dioxygenase
  • Kynurenine