Biomarkers of Post-COVID Depression

Abstract

The COVID-19 pandemic is spreading around the world and 187 million people have already been affected. One of its after-effects is post-COVID depression, which, according to the latest data, affects up to 40% of people who have had SARS-CoV-2 infection. A very important issue for the mental health of the general population is to look for the causes of this complication and its biomarkers. This will help in faster diagnosis and effective treatment of the affected patients. In our work, we focused on the search for major depressive disorder (MDD) biomarkers, which are also present in COVID-19 patients and may influence the development of post-COVID depression. For this purpose, we searched PubMed, Scopus and Google Scholar scientific literature databases using keywords such as ‘COVID-19’, ‘SARS-CoV-2’, ‘depression’, ‘post-COVID’, ‘biomarkers’ and others. Among the biomarkers found, the most important that were frequently described are increased levels of interleukin 6 (IL-6), soluble interleukin 6 receptor (sIL-6R), interleukin 1 β (IL-1β), tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2), soluble interleukin 2 receptor (sIL-2R), C-reactive protein (CRP), Monocyte Chemoattractant Protein-1 (MCP-1), serum amyloid a (SAA1) and metabolites of the kynurenine pathway, as well as decreased brain derived neurotrophic factor (BDNF) and tryptophan (TRP). The biomarkers identified by us indicate the etiopathogenesis of post-COVID depression analogous to the leading inflammatory hypothesis of MDD.

Post-COVID-19 Syndrome: Involvement and Interactions between Respiratory, Cardiovascular and Nervous Systems

“…Particularly, cytokine storm and increased inflammatory factors contribute to the augmentation of the permeability of the blood-brain barrier. The effect is a reduction in tryptophan and serotonin circulating levels and an augmentation of toxics such as kynurenine, quinolinic acid or 3-hydroxykynurenine [99]. These variations facilitate neurotoxicity, neurodegeneration and reduction in neurogenesis and synaptic plasticity [99].…”

“…The effect is a reduction in tryptophan and serotonin circulating levels and an augmentation of toxics such as kynurenine, quinolinic acid or 3-hydroxykynurenine [99]. These variations facilitate neurotoxicity, neurodegeneration and reduction in neurogenesis and synaptic plasticity [99]. Specifically, inflammation determines endothelial alterations and migration of leukocytes across the blood-brain barrier [93].…”

Ordering Knowledge in the Markers of Psychiatric/Mental Disorders

“…It seems that the inflammatory characteristic of the onset of various psychiatric illnesses (schizophrenia (SCH), anxiety (ANX), or affective disorders, such as major depression (MDD) and bipolar disorder (BD), as described by the authors of the Special Issue [1][2][3][4][5][6]) is similar, which seems to be due to the hyperactivated hypothalamic-pituitary-adrenal stress (HPA) axis. The differences between psychotic, anxiety, and affective disorders in the inflammatory state appear to start with a decrease in HPA activity.…”

“…The increased cytokine levels may potentially reduce frontal brain activity, which may mimic depressive symptoms in vulnerable patients. High values of IL-6, CRP, and TNF may also be involved in or be the reason for treatmentresistant depression (TRD) and more somatic symptoms, but they may be used to predict the level of depressive response in post-COVID-19 patients [1,3,12]. Higher air humidity (the concentration of water vapour present in the air) around depressive persons were compared to non-depressive persons, and correlations between humidity with symptoms of depression were found, whereas no other weather condition difference, nor its correlation with depressive symptoms, were noted (Białystok Plus study described in [13,14]; meteorological data in preparation).…”

Increased Kynurenine Indicates a Fatal Course of COVID-19

“…Evidence exists, that the KYN pathway is also involved in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [ 18 , 19 ]. Herein, an altered TRP metabolism may disturb an effective immune response, involved in oxidative stress generation [ 20 ], and promote long-term symptoms in survivors of coronavirus disease 2019 (COVID-19) [ 21 ] including post COVID depression [ 22 ].…”