This study presented clinical, radiological and laboratory features of cytotoxic lesions of the corpus callosum (CLOCCs) in eight COVID-19 patients.
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Acute COVID-19 & Nervous system
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In a mouse model of transient focal brain ischemia, the recombinant SARS-CoV-2 spike protein disrupted the RAAS balance, increased coagulation, and decreased fibrinolysis, which worsened ischemic stroke outcome
This study provides new evidence that SARS-CoV-2 S protein injection given to hACE2 KI mice seven days before transient focal brain ischemia disrupted the RAAS balance by increasing Ang II/AT1R signaling in the brain’s cells at the expense of the Ang II/AT2R protective arm.
SARS-CoV-2 infection in vitro triggered the inflammation and senescence pathways in A9 dopaminergic neurons (mostly affected by Parkinson’s disease in the substantia nigra) derived from human pluripotent stem cells. Increased risk of viral-induced parkinsonism?
This study demonstrated selective in vitro vulnerability of A9 DA neurons derived from human pluripotent stem cells to SARS-CoV-2 infection and the associated inflammatory and cellular senescence response.
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“Neurotoxin-like region” of the SARS-CoV-2 spike protein modulates nicotinic acetylcholine receptors (with a high preference for the α7 subtype linked with aggression, anxiety, and depression)
Neurotoxin-like region of the SARS-CoV-2 interact with the nicotinic acetylcholine receptors. The α7 nAChR is a target for the SARS-CoV-2.
COVID-19-associated unilateral encephalitis (case report)
A rare case of COVID-19-associated unilateral encephalitis, characterized by severe involvement of the left cerebral hemisphere.
The inoculation of the SARS-CoV-2 S1 protein in the olfactory cavity resulted in brain inflammation and reduced acetylcholine level in the mouse brain
This investigation shows a link between the S1 subunit of the spike protein, brain inflammation, and reduced production of acetylcholine.
The role of hypothalamic circuits and the median eminence, not completely protected by the blood-brain barrier, in brain infection with SARS-CoV-2
Some CNS structures, like the choroid plexus and the circumventricular organs including the hypothalamus, are not completely protected by the BBB and can serve as virus entry points.
The neurons of the peripheral nervous system serve as an alternative route for SARS-CoV-2 invasion of the central nervous system, independent of viremia
After intranasal SARS-CoV-2 inoculation, the findings demonstrated susceptibility of sensory and autonomic neurons of the PNS and CNS to productive infection with SARS-CoV-2 through direct neural invasion that preceded viremia.
SARS-CoV-2 can infect and replicate in human motor neurons differentiated from induced pluripotent stem cells
SARS-CoV-2 is able to infect and replicate in an in vitro model of human motor neurons differentiated from induced pluripotent stem cells.
SARS-CoV-2 spike protein and its receptor-binding domain stimulate human microglia through different receptors to secrete various proinflammatory mediators
Recombinant full-length S protein and its RBD stimulate human microglia via activation of different receptors. These findings confirmed that the SARS-CoV-2 S protein contributes to neuroinflammation via several mechanisms involved in CNS pathologies.
The Wuhan wild-type strain and five variants of SARS-CoV-2 differently affect the viability of various brain cells (pericytes, astrocytes, endothelial cells, and microglia) and the integrity of the blood-brain barrier
The wild-type Wuhan strain and five variants Alpha, Beta, Delta, Eta, and Omicron, carrying specific mutations that modulate their infectivity and transmissibility, affect the brain cells and the blood-brain barrier differently.
The presence of the SARS-CoV-2 S1 protein in the skull and meninges might show an alternative route for S protein entry into the CNS
The findings of this study suggest an alternative route for the SARSCoV-2 S protein entry into the CNS, wherein it might reache first the skull marrow and meninges before entering the brain.
