Potential Neuroprotective Effect of Cannabinoids in COVID-19 Patients.

Curr Top Med Chem

Division de Neurociencias, Instituto Nacional de Rehabilitación, Secretaría de Salud, Mexico City, 14389, Mexico.

Published: August 2022

AI Article Synopsis

  • The SARS-CoV-2 pandemic, which started in early 2020, is known for causing respiratory issues, but it also leads to neurological problems that stem from either direct damage or inflammatory responses in the body.
  • Proposed causes for neurological damage include cerebrovascular diseases and autoimmune reactions linked to COVID-19.
  • Some studies suggest that cannabinoids could offer neuroprotective benefits in COVID-19 patients by activating the endocannabinoid system, which may help reduce viral effects and inflammatory responses in the brain.

Article Abstract

The global pandemic caused by the SARS-CoV-2 virus began in early 2020 and is still present. The respiratory symptoms caused by COVID-19 are well established. However, neurological manifestations that may result from direct or indirect neurological damage after SARS-CoV-2 infection have been reported frequently. The main proposed pathophysiological processes leading to neurological damage in COVID-19 are cerebrovascular disease and indirect inflammatory/ autoimmune origin mechanisms. A growing number of studies confirm that neuroprotective measures should be maintained in COVID-19 patients. On the other hand, cannabinoids have been the subject of various studies that propose them as potentially promising drugs in chronic neurodegenerative diseases due to their powerful neuroprotective potential. In this review, we addresses the possible mechanism of action of cannabinoids as a neuroprotective treatment in patients infected by SARS-CoV-2. The endocannabinoid system is found in multiple systems within the body, including the immune system. Its activation can lead to beneficial results, such as a decrease in viral entry, a reduction of viral replication, and a reduction of pro-inflammatory cytokines such as IL-2, IL-4, IL-6, IL-12, TNF-α, or IFN-c through CB2R expression induced during inflammation by SARS-CoV-2 infection in the central nervous system.

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Source
http://dx.doi.org/10.2174/1568026622666220405143003DOI Listing

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