tetano
Editor, Senior Moderator
Life Sci
. 2022 Sep 20;120981.
doi: 10.1016/j.lfs.2022.120981. Online ahead of print.
SARS-CoV-2 mediated neurological disorders in COVID-19: Measuring the pathophysiology and immune response
Pi-Ching Hsu[SUP] 1 [/SUP], Md Shahed-Al-Mahmud[SUP] 2 [/SUP]
Affiliations
Abstract
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 upregulate in SARS-CoV-2 infected aged patients' brains 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.
Keywords: COVID-19; Immune response; Neurological complications; Pathogenesis; SARS-CoV-2.
. 2022 Sep 20;120981.
doi: 10.1016/j.lfs.2022.120981. Online ahead of print.
SARS-CoV-2 mediated neurological disorders in COVID-19: Measuring the pathophysiology and immune response
Pi-Ching Hsu[SUP] 1 [/SUP], Md Shahed-Al-Mahmud[SUP] 2 [/SUP]
Affiliations
- PMID: 36150465
- PMCID: PMC9490490
- DOI: 10.1016/j.lfs.2022.120981
Abstract
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 upregulate in SARS-CoV-2 infected aged patients' brains 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.
Keywords: COVID-19; Immune response; Neurological complications; Pathogenesis; SARS-CoV-2.