Frontiers | The impact of COVID-19 on accelerating of immunosenescence and brain aging
COVID-19 induces chronic inflammation, immunosenescence, and neuroinflammation.
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.
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”
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.”