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Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19

Exploring the Persistence of the Spike Protein along the Skull-Meninges-Brain Axis and the Neurological Effects of COVID-19

This analysis is supported by numerous videos and illustrations.

·cell.com·
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19
SARS-CoV-2 infection of the brain: the K18-hACE2 mouse model to illustrate the role and response of the vasculature in neurotropic viral infection
SARS-CoV-2 infection of the brain: the K18-hACE2 mouse model to illustrate the role and response of the vasculature in neurotropic viral infection

Researchers used mouse model to study how SARS-CoV-2 infects the brain.

The virus targets neurons but spares blood vessels, triggering neuroinflammation and blood-brain barrier dysfunction.

·biorxiv.org·
SARS-CoV-2 infection of the brain: the K18-hACE2 mouse model to illustrate the role and response of the vasculature in neurotropic viral infection
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19

Evidence that a COVID-19 infection can induce neurological sequelae.

The SARSCoV2 spike protein can persist in the brain—skull bone marrow and meninges—to induce neurologic damage

SARS-CoV-2 spike protein accumulates & persists in the body for years after infection, especially in the skull-meninges-brain axis, potentially driving long COVID. mRNA vaccines help but cannot stop it.

In mice, it caused inflammation, anxiety, and worsened brain injuries. Vaccines reduced but did not fully eliminate it.

SARS-CoV-2 spike protein persists in the skull-meninges-brain axis in COVID-19 patients•Spike protein is sufficient to induce brain pathological and behavioral changes in mice•Spike protein enhances brain vulnerability and exacerbates neurological damage in mice•mRNA vaccines reduce, but do not eliminate, the spike burden
·cell.com·
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19
Recorded this video on the microscope yesterday. A single infected cell arrives on the brain inside a blood vessel. Don't underestimate how much neuroinflammation one infected cell can cause.
Recorded this video on the microscope yesterday. A single infected cell arrives on the brain inside a blood vessel. Don't underestimate how much neuroinflammation one infected cell can cause.

“Recorded this video on the microscope yesterday. A single #SARSCoV2 infected cell arrives on the brain inside a blood vessel. Don't underestimate how much neuroinflammation one infected cell can cause. Brain-vascular-immune interface is the future of neuroscience #NeuroCovid”

·x.com·
Recorded this video on the microscope yesterday. A single infected cell arrives on the brain inside a blood vessel. Don't underestimate how much neuroinflammation one infected cell can cause.
Pioneering discovery and therapeutics at the brain-vascular-immune interface
Pioneering discovery and therapeutics at the brain-vascular-immune interface

A new paper in Cell, “Pioneering discovery and therapeutics at the brain-vascular-immune interface,” describes COVID-19 as a neurological disease alongside multiple sclerosis, Alzheimer’s, stroke and traumatic brain injury.

“COVID-19 can accelerate progression of dementia and induce BBB disruption and inflammatory blood clots causally linked with neuroinflammation and neuronal loss.8 In neurodevelopmental disorders, prematurity and perinatal hypoxia that trigger brain hemorrhage and BBB disruption are risk factors for cerebral palsy, intellectual disability, and autism. Collectively, these risk factors highlight the interconnected vascular and immune triggers of neurological diseases.”

·cell.com·
Pioneering discovery and therapeutics at the brain-vascular-immune interface