Neurological and Neuropsychological Changes Associated with SARS-CoV-2 Infection: New Observations, New Mechanisms.
Muhammad Ali HaidarHussam JourdiZeinab Haj HassanOhanes AshekyanManal FardounZena WehbeDina MaalikiMaya WehbeStefania MondelloSamar AbdelhadyShima ShahjoueiMaya BizriYehia MechrefMark S GoldGhassan DbaiboHassan ZaraketAli H EidFiras H KobeissyPublished in: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry (2021)
SARS-CoV-2 infects cells through angiotensin-converting enzyme 2 (ACE2), a ubiquitous receptor that interacts with the virus' surface S glycoprotein. Recent reports show that the virus affects the central nervous system (CNS) with symptoms and complications that include dizziness, altered consciousness, encephalitis, and even stroke. These can immerge as indirect immune effects due to increased cytokine production or via direct viral entry into brain tissue. The latter is possible through neuronal access via the olfactory bulb, hematogenous access through immune cells or directly across the blood-brain barrier (BBB), and through the brain's circumventricular organs characterized by their extensive and highly permeable capillaries. Last, the COVID-19 pandemic increases stress, depression, and anxiety within infected individuals, those in isolation, and high-risk populations like children, the elderly, and health workers. This review surveys the recent updates of CNS manifestations post SARS-CoV-2 infection along with possible mechanisms that lead to them.
Keyphrases
- angiotensin converting enzyme
- cerebral ischemia
- blood brain barrier
- sars cov
- respiratory syndrome coronavirus
- angiotensin ii
- induced apoptosis
- resting state
- white matter
- healthcare
- subarachnoid hemorrhage
- cell cycle arrest
- public health
- atrial fibrillation
- young adults
- binding protein
- mental health
- brain injury
- health information
- risk factors
- oxidative stress
- health promotion
- cell death
- cell proliferation
- endoplasmic reticulum stress
- human health
- social media
- adverse drug