The respiratory illness COVID-19 started a global pandemic in 2019 and continued until 2020. Globally, the epidemic claimed the lives of around 480,000 persons and affected 9.5 million people. SARS-CoV-2 is the primary cause of this outbreak. SARS-CoV-2 is an RNA virus that is encapsulated and can infect multiple organs. It can enter the host through spike proteins. This epidemic had a serious impact on the brain as well. The recovered patients experienced neurological problems following COVID-19, neuropsychiatric symptoms, cognitive impairment, and difficulty concentrating. Nonetheless, the primary cause of all these clinical disorders or changes in psycho-behavioral patterns is consistently neuroinflammation. The neurological characteristics of COVID-19 patients and the neuroinflammatory effects of SARS-CoV-2 infection will be the main topics of this review. Studies have indicated that the brain inflammation caused by COVID-19 may be partly attributed to the overproduction of free radicals such as ROS and NO as well as the downregulation of antioxidant enzymes. Furthermore, cytokine storm, which is brought on by inflammatory cytokines like IL-1β, IFN-γ, and IL-6, may be the cause of major depressive disorder (MDD). Thus, it is clear from this analysis how critical it is to manage the harmful neuroinflammatory effects of SARS-CoV-2 infection, which ultimately result in the death of neurons and neurological impairment. Considering all the information, it is possible to conclude that controlling these inflammatory effects effectively may be a useful tactic for preserving normal brain function.
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Rajen Dey (2024) studied this question.
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