SARS-CoV-2 mediated neurological disorders in COVID-19: Measuring the pathophysiology and immune response

The emergence of beta-coronavirus SARS-CoV-2 gets entry into its host cells by recognizing angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRESS2) receptors, which are responsible for coronavirus diseases-2019 (COVID-19). Global communities have been affected by COVID-19, especially caused the neurological complications and other critical medical issues. COVID-19 associated complications appear in aged people with underlying neurological states, especially in Parkinson's disease (PD) and Alzheimer's disease (AD). ACE2 receptors abundantly expressed in dopamine neurons may worsen the motor symptoms in PD and upregulates in SARS-CoV-2 infected aged patients' brain with AD. Immune-mediated cytokines released in SARS-CoV-2 infection lead to an indirect immune response that damages the central nervous system. Extreme cytokines release (cytokine storm) occurs due to aberrant immune pathways, and activation in microglial propagates CNS damage in COVID-19 patients. Here, we have explored the pathophysiology, immune responses, and long-term neurological impact on PD and AD patients with COVID-19. It is also a crucial step to understanding COVID-19 pathogenesis to reduce fatal outcomes of neurodegenerative diseases.