Depressive and Neurocognitive Disorders in the Context of the Inflammatory Background of COVID-19

Abstract

The dysfunctional effects of the coronavirus disease 2019 (COVID-19) infection on the nervous system are established. The manifestation of neuropsychiatric symptoms during and after infection is influenced by the neuroinvasive and neurotrophic properties of SARS-CoV-2 as well as strong inflammation characterised by a specific “cytokine storm”. Research suggests that a strong immune response to a SARS-CoV-2 infection and psychological stressors related to the pandemic may cause chronic inflammatory processes in the body with elevated levels of inflammatory markers contributing to the intensification of neurodegenerative processes. It is suggested that neuroinflammation and associated central nervous system changes may significantly contribute to the etiopathogenesis of depressive disorders. In addition, symptoms after a COVID-19 infection may persist for up to several weeks after an acute infection as a post-COVID-19 syndrome. Moreover, previous knowledge indicates that among SSRI (selective serotonin reuptake inhibitor) group antidepressants, fluoxetine is a promising drug against COVID-19. In conclusion, further research, observation and broadening of the knowledge of the pathomechanism of a SARS-CoV-2 infection and the impact on potential complications are necessary. It is essential to continue research in order to assess the long-term neuropsychiatric effects in COVID-19 patients and to find new therapeutic strategies.

Mapping the structure of depression biomarker research: A bibliometric analysis

“…Previous studies have suggested that the contribution of COVID-19 to the increased prevalence of depression has been attributed to population shocks, social isolation, quarantines and uncertainty about the future (60). It has also been suggested that the association of COVID-19 with depression is inextricably linked to neuroinflammation (61,62). da Silva Lopes L et al noted that due to the action of inflammatory cytokines and the presence of cell surface ACE-2 receptors, COVID-19 survivors may be more susceptible to depression (63).…”

Potential Role of the Antidepressants Fluoxetine and Fluvoxamine in the Treatment of COVID-19

“…Results of this study are therefore probably partially related to the antidepressant effect of fluoxetine and are not necessarily linked to the COVID-19 pathology itself. Overall, in a clinical context, the improvement of depression and anxiety should be considered an important confounder in relation to somatic improvement, because psychiatric improvement has been shown to have a direct effect on somatic endpoints [ 55 , 56 ]. Therefore, changes in depressive and anxiety symptoms should also be screened in future studies assessing the effectiveness of antidepressants in COVID-19 patients, making the control of this cofactor possible.…”

Treatment paradigms in Parkinson's Disease and Covid-19

“…However, newer data suggests that the indication for antidepressants should be re-examined ( Wada et al, 2001 ), as fluoxetine, sertraline and venlafaxine have been successfully used in various case reports ( Dubovsky et al, 2012 ). Fluoxetine, in particular, has been shown to be a promising drug in the context of Covid-19 due to reported anti-inflammatory properties ( Dąbrowska, Galińska-Skok, & Waszkiewicz, 2021 ). TCAs like nortriptyline and desipramine have been labeled as “likely efficacious” and “clinically useful” to treat depression in PwP ( Seppi et al, 2019 ) and could be considered also for anxiety in PD, although they should be avoided in patients with suicidal ideation or cardiovascular problems ( Prediger, Matheus, Schwarzbold, Lima, & Vital, 2012 ).…”