COVID-19, Oxidative Stress, and Neuroinflammation in the Depression Route.
Maiqueli Eduarda Dama MingotiAmanda Gollo BertolloJúlia Leão Batista SimõesGabriel Rossi FranciscoMargarete Dulce BagatiniZuleide Maria IgnácioPublished in: Journal of molecular neuroscience : MN (2022)
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.
Keyphrases
- oxidative stress
- coronavirus disease
- major depressive disorder
- sars cov
- lipopolysaccharide induced
- traumatic brain injury
- bipolar disorder
- dna damage
- lps induced
- cerebral ischemia
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- cognitive impairment
- inflammatory response
- early onset
- depressive symptoms
- sleep quality
- spinal cord
- physical activity
- ms ms
- neuropathic pain
- subarachnoid hemorrhage
- blood brain barrier