The Effect of Antidepressant Treatment on Neurocognitive Functions, Redox and Inflammatory Parameters in the Context of COVID-19.

Publication date: Nov 12, 2023

Inflammation is an important component of the etiopathology of depression that uses oxidative and nitrosative stress (O&NS) and elevated inflammatory markers. SARS-CoV-2 infection is also associated with abnormal inflammatory processes, which may impair effective treatment of depression in COVID-19 survivors. In the presented study, thirty-three hospitalized patients with major depressive disorder (MDD) were started on antidepressant treatment, and twenty-one were re-evaluated after 4-6 weeks. The control group consisted of thirty healthy volunteers. All participants underwent neuropsychiatric evaluation, biochemical blood and urine analyses. The results of the research demonstrated positive correlations of the Hamilton Depression Rating Scale (HAM-D) scores with serum catalase (CAT) and urinary S-Nitrosothiols levels, and the Beck Depression Inventory (BDI) scores with serum reduced glutathione (GSH) and superoxide dismutase (SOD) levels. Depressed patients with a history of COVID-19 prior to the treatment had higher urinary nitric oxide (NO) levels and lower serum glutathione peroxidase (GPx) levels. In the control group, COVID-19 survivors had higher levels of urinary N-formylkynurenine (NFK). Our results suggest that the antidepressant treatment has a modulating effect on O&NS, reduces depressive symptoms and improves cognitive functions The present study does not indicate that clinical response to antidepressant treatment is associated with COVID-19 history and baseline SARS-CoV-2 antibody levels. Nevertheless, further research in this area is needed to systematize antidepressant treatment in COVID-19 survivors.

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Concepts Keywords
Antibody antidepressant treatment
Cat antidepressants
Thirty COVID-19
Urinary CRP
Volunteers D-dimers
neurocognitive functions
oxidative stress
SARS-CoV-2 antibodies


Type Source Name
disease MESH COVID-19
disease MESH Inflammation
disease MESH oxidative and nitrosative stress
pathway REACTOME SARS-CoV-2 Infection
disease VO effective
disease MESH major depressive disorder
disease IDO blood
disease VO Catalase
drug DRUGBANK Glutathione
disease IDO history
drug DRUGBANK Nitric Oxide
disease MESH nitrosative stress
disease MESH uncertainty
disease MESH affective disorders
disease MESH mental disorders
disease MESH depressive disorder
disease VO population
disease MESH etiology
drug DRUGBANK Coenzyme M
drug DRUGBANK Serotonin
disease MESH cytokine storm
disease MESH neuroinflammation
disease MESH infection
disease IDO production
drug DRUGBANK Oxygen
drug DRUGBANK Nitrogen
disease MESH death
disease MESH cognitive impairment
disease MESH neurodegenerative disorders
disease VO dose
drug DRUGBANK Fluoxetine
drug DRUGBANK Vortioxetine
disease VO effectiveness
disease IDO process
disease MESH obesity
drug DRUGBANK Ethanol
disease MESH comorbidity
drug DRUGBANK Indoleacetic acid
drug DRUGBANK Dihydrostreptomycin
drug DRUGBANK Protein S human
disease MESH olfactory impairment
drug DRUGBANK Escitalopram
drug DRUGBANK Sertraline
drug DRUGBANK Duloxetine
drug DRUGBANK Venlafaxine
drug DRUGBANK Amitriptyline
drug DRUGBANK Mirtazapine
drug DRUGBANK Bupropion
drug DRUGBANK Methionine
drug DRUGBANK Etoperidone
drug DRUGBANK Creatinine
drug DRUGBANK L-Alanine
drug DRUGBANK Cholesterol
disease VO USA
drug DRUGBANK L-Tryptophan
disease VO company
disease IDO assay
drug DRUGBANK Human Serum Albumin
drug DRUGBANK Epinephrine
drug DRUGBANK Hydrogen peroxide
drug DRUGBANK Nadide
drug DRUGBANK Phosphate ion
drug DRUGBANK Sulfanilamide
drug DRUGBANK Ethylenediamine
disease MESH education levels
disease MESH Taste disorders

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