Serum Brain-Derived Neurotrophic Factor (BDNF) in COVID-19 Patients and its Association with the COVID-19 Manifestations

Abstract

COVID-19 is a systematic disease that frequently implies neurological and non-neurological manifestations, predominantly by inducing hypoxia. Brain-derived neurotrophic factor (BDNF) is a key factor in regulating functions of nervous and respiratory systems and has been strongly related to hypoxia. Therefore, this study planned to investigate BDNF association with the COVID-19 manifestations especially neurological impairments and the infection-induced hypoxia. We enrolled sixty-four COVID-19 patients and twenty-four healthy individuals in this study. Patients were divided into two groups, with and without neurological manifestations, and their serum BDNF levels were measured by enzyme-linked immunosorbent assay (ELISA). COVID-19 patients had significantly lower BDNF levels than healthy individuals ( p = 0.023). BDNF levels were significantly lower in patients with neurological manifestations compared to healthy individuals ( p = 0.010). However, we did not observe a statistically significant difference in BDNF levels between patients with and without neurological manifestations ( p = 0.175). BDNF’s levels were significantly lower in patients with CNS manifestations ( p = 0.039) and higher in patients with fever ( p = 0.03) and dyspnea ( p = 0.006). Secondly, BDNF levels have a significant negative association with oxygen therapy requirement ( p = 0.015). These results strongly suggest the critical association between dysregulated BDNF and hypoxia in promoting COVID-19 manifestations, particularly neurological impairments. Supplementary Information The online version contains supplementary material available at 10.1007/s12031-022-02039-1.

Is SARS-CoV-2 a Risk Factor of Bipolar Disorder?—A Narrative Review

“…In a study involving 64 COVID-19 (+) patients there was a significant reduction in BDNF level among patients as compared to the control group. This difference was greatest in a group with the neurological manifestation of COVID-19, and smaller in patients with only fever and dyspnea [ 154 ]. A decrease in BDNF level in COVID-19 patients depending on their condition has also been observed in other studies and it was negatively correlated with the severity of the patients’ condition, and its normalization followed the improvement of the clinical condition [ 155 , 156 ].…”

“…Most studies seem to confirm that COVID-19 infection causes a decrease in BDNF levels [ 154 , 155 , 156 ]. These results, however, are not consistent in all cases and there are studies that do not show a decrease in BDNF, or even its increase among patients who developed “long-COVID” [ 160 ].…”

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

“…Altered expression of genes include CX3CR1 [666], S100A12 [667], CSF2 [668], MPO (myeloperoxidase) [669], CD5L [670], F11 [671], S100A8 [672], PGLYRP1 [673], VEGFD (vascular endothelial growth factor D) [674], CXCL11 [373], BPI (bactericidal permeability increasing protein) [675], CXCL10 [676], S100A9 [677], CXCR1 [678], CXCR2 [679], ABCA3 [680], CD36 [681], SHH (sonic hedgehog signaling molecule) [682], TLR3 [683], CLEC4D [684], CCR2 [685], NEK7 [686], TLR7 [687], CCRL2 [688] and CAV1 [689] accelerates pneumonia progression. CX3CR1 [666], CD177 [690], PF4 [691], FFAR2 [692], MPO (myeloperoxidase) [693], F11 [694], S100A8 [695], VEGFD (vascular endothelial growth factor D) [674], IL1A [696], BPI (bactericidal permeability increasing protein) [697], AQP4 [698], BDNF (brain derived neurotrophic factor) [699], CXCL10 [700], RNASE2 [701], FCGR3B [702], S100A9 [703], IL1B [704], CXCR2 [705], GPIHBP1 [294], CD36 [706], TRIB3 [707], PCSK9 [708], FGF2 [709], FASN (fatty acid synthase) [710], PNPLA3 [711], HSPA6 [712], VIP (vasoactive intestinal peptide) [713], TLR3 [683], ADRB1 [328], SPOCK2 [714], TLR8 [715], CCR2 [716], IFIT3 [717], NEK7 [718], TLR7 [687], EFNB2 [719], CAV1 [720], CR1 [721] and AQP5 [722] plays essential roles in viral respiratory diseases. Previous study confirmed that CX3CR1 [723], S100A12 [724], CD177 [725], PF4 [726], MPO (myeloperoxidase) [727], CD5L [728], F11 […”

Impact of COVID-19 on Neuropsychiatric Disorders

“…Overall, research in this area is advancing. For instance, some studies have found an association between low neurotrophic factors and COVID-19-related neuropsychiatric complications [ 99 ]; thus, neurotrophic drugs such as cerebrolysin may serve as a potential therapeutic approach to improve neuropsychiatric manifestations of COVID-19 [ 100 ]. Clearly, more research studies and clinical trials are needed in this regard.…”