Neurology & Neurophysiology

Biography

Biography: Maryna Skok

Abstract

COVID-19 caused by SARS-Cov-2 infection affects multiple organs and tissues including the brain. PostCOVID patients often suffer from cognitive disorders like depression, intellectual weakness and memory loss. The fragment 674-685 of SARS-Cov-2 spike protein is homologous to the fragment 27-37 of α-cobratoxin underlying its interaction with α7 nicotinic acetylcholine receptors (nAChRs) known to be involved in memory and cognition. Both in silico and biochemical studies demonstrated direct interaction of 674-685 spike protein fragment with the portion 179-190 of α7 nAChR. We immunized mice with 674-685 peptide coupled to a protein carrier and observed a decrease of episodic memory measured in novel object recognition test starting from day 14 after initial immunization that coincided with the first peak of (674-685)-specific antibodies in the blood. The antibodies of such specificity were also found in the brain of mice sacrificed on day 14 after the second immunization. The antibody presence was accompanied with the decrease of α7 nAChRs and increased levels of pro-inflammatory cytokines IL-1β and TNFα in the brain. Choline prevented (674-685)-specific antibody binding to BSA-coupled (674-685) peptide indicating that the antibody could bind choline. When injected regularly in (674-685)-immunized mice choline prevented memory loss and the decrease of α7 nAChRs in the brain. Finally, the antibodies specific to (674-685) spike protein fragment were detected in the blood of COVID-19 patients 2 to 3 months after recovery and their level depended on the severity of the disease. The data obtained allow suggesting that post-COVID memory impairment is caused by the antibodies directed to (674-685) fragment of SARS-Cov-2 spike protein. Choline treatment/consumption may be helpful to overcome neurological post-COVID complications