COVID-19 AND NEUROLOGICAL SEQUELAE: VITAMIN D AS A POSSIBLE NEUROPROTECTIVE AND/OR NEUROREPARATIVE AGENT

GARCÍA SEBASTIÁN; VIRNA MARTÍN GIMENÉZ; FRANCISCO BARRANTES; MICHAEL F. HOLICK; WALTER MANUCHA

LIFE SCIENCES

PERGAMON-ELSEVIER SCIENCE LTD

Lugar: Amsterdam; Año: 2022 vol. 297

0024-3205

SARS-CoV-2, the ethiological agent of the current COVID-19 pandemic, belongs to a broad family of coronaviruses that also affect humans. SARS-CoV-2 infection usually leads to bilateral atypical pneumonia with significant impairment of respiratory function. However, the infectious capacity of SARS-CoV-2 is not limited to the respiratory system, but may also affect other organs such as the brain and other vital organs. The central nervous system may be affected by cell damage due to direct invasion or indirect virus-related effects leading to a neuroinflammatory response. These processes may be associated with a decrease in the activity of angiotensin II converting enzyme (ACE2), the canonical cell-surface receptor for SARS-CoV-2. This enzyme regulates neuroprotective and neuroimmunomodulatory functions and can neutralize both inflammation and oxidative stress generated at the cellular level. Additionally, there is evidence on the association between vitamin D deficiency and predisposition to the development of severe forms of COVID-19 and, consequently, of neurological and neuropsychiatric sequelae. This is because vitamin D has the ability to down-modulate the effects of neuroinflammatory cytokines, among other anti-inflammatory/immunomodulatory effects, thus attenuating harmful consequences of COVID-19. This review critically analyzes current evidence supporting the notion that vitamin D may act as a neuroprotective and neuroreparative agent against the neurological sequelae derived from COVID-19.