COVID-19 Pandemic and Neurocognitive Process: New Scenarios for Understanding and Treatment

Abstract

COVID-19 disease was defined as a disease of primary respiratory system. However, symptoms associated with central nervous system were detected in approximately 2/3 of the hospitalized patients. The rate of ischemic cerebrovascular diseases is higher in central nervous system. In addition, hemorrhagic cerebrovascular diseases, encephalitis and/or encephalopathy are the other diseases. Complex pathogenesis was demonstrated in the central nervous system diseases associated with SARS-CoV-2. It was reported that SARS-CoV-2 virus could directly invade the central nervous system, especially via the olfactory nerves or the haematological pathway. As a result, endothelial cells, pericytes and/or neurons can be infected (direct pathway). Another mechanism is central nervous system deficit resulting from peripheral immune reactivation (indirect pathway). All these etiopathogenetic results support that COVID-19 disease is associated with cognitive dysfunction. Cerebral hypoperfusion associated with vascular endothelial structures is the main factor in the etiopathogenesis. It was reported that COVID-19 disease induced amyloid-β (Aβ) and α-synuclein phosphorylation. Besides, it was detected that this process was associated with tau and TDP-43 pathology. “Cognitive COVID-19” is a term that describes acute and long-term cognitive changes in people infected with SARS-CoV-2. Encephalopathy, delirium and cognitive disorders are most frequently detected. In this chapter, the clinical and etiopathogenetic processes of cognitive dysfunction after COVID-19 disease were evaluated. In addition, the disease, disease process and treatment were evaluated in general.