Covid and Brain Damage

Covid and Brain Damage

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Cognitive dysfunctions in the course of SARS‑CoV‑2 virus infection, including NeuroCOVID, frontal syndrome and cytokine storm (Review)
Cognitive dysfunctions in the course of SARS‑CoV‑2 virus infection, including NeuroCOVID, frontal syndrome and cytokine storm (Review)
𝘾𝙤𝙜𝙣𝙞𝙩𝙞𝙫𝙚 𝙙𝙮𝙨𝙛𝙪𝙣𝙘𝙩𝙞𝙤𝙣𝙨 𝙞𝙣 𝙩𝙝𝙚 𝙘𝙤𝙪𝙧𝙨𝙚 𝙤𝙛 𝙎𝘼𝙍𝙎‑𝘾𝙤𝙑‑2 𝙫𝙞𝙧𝙪𝙨 𝙞𝙣𝙛𝙚𝙘𝙩𝙞𝙤𝙣, 𝙞𝙣𝙘𝙡𝙪𝙙𝙞𝙣𝙜 𝙉𝙚𝙪𝙧𝙤𝘾𝙊𝙑𝙄𝘿, 𝙛𝙧𝙤𝙣𝙩𝙖𝙡 𝙨𝙮𝙣𝙙𝙧𝙤𝙢𝙚 𝙖𝙣𝙙 𝙘𝙮𝙩𝙤𝙠𝙞𝙣𝙚 𝙨𝙩𝙤𝙧𝙢
·spandidos-publications.com·
Cognitive dysfunctions in the course of SARS‑CoV‑2 virus infection, including NeuroCOVID, frontal syndrome and cytokine storm (Review)
NF-κB links COVID-19 to PD | JIR
NF-κB links COVID-19 to PD | JIR
Role of Inflammation in the Development of COVID-19 to Parkinson’s Disease
·dovepress.com·
NF-κB links COVID-19 to PD | JIR
Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols
Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols

“The nervous system, particularly the brain, can become infected by SARS-CoV-2 early in the course of COVID-19 via viral access through the cribriform plate located at the upper part of the nose.. this route is more ominous than previously thought. The pits of the cribriform plate and areas beneath the olfactory bulb including potential spaces such as the air sinuses can be a reservoir for not only viral persistence, but also its replication.. the upper part of the nose and the structures surrounding it appear to be ideal sites for access to the CNS (central nervous system).. This can cause a low-grade inflammation in the meninges and deeper tissues in the neuronal environment triggering neuroinflammation.. [This can cause] Symptoms such as brain fog, cognitive deficits, prolonged anosmia, memory deficits, and deposition of amyloid-like fibrils that cause premature aging in patients with long COVID.."

It's certainly ominous that SARS-CoV-2 can infect my brain instantly and silently.”

·link.springer.com·
Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols
Cell invasive amyloid assemblies from SARS-CoV-2 peptides can form multiple polymorphs with varying neurotoxicity
Cell invasive amyloid assemblies from SARS-CoV-2 peptides can form multiple polymorphs with varying neurotoxicity

𝘼𝙢𝙮𝙡𝙤𝙞𝙙 𝙖𝙜𝙜𝙧𝙚𝙜𝙖𝙩𝙚𝙨 𝙛𝙧𝙤𝙢 𝙎𝘼𝙍𝙎-𝘾𝙤𝙑-2 𝙥𝙚𝙥𝙩𝙞𝙙𝙚𝙨 𝙧𝙚𝙖𝙙𝙞𝙡𝙮 𝙚𝙣𝙩𝙚𝙧 𝙣𝙚𝙪𝙧𝙤𝙣𝙖𝙡 𝙘𝙚𝙡𝙡𝙨, 𝘢𝘯𝘥 𝘵𝘩𝘪𝘴 𝘤𝘢𝘶𝘴𝘦𝘴 𝘢 𝘳𝘦𝘥𝘶𝘤𝘵𝘪𝘰𝘯 𝘪𝘯 𝘵𝘩𝘦𝘪𝘳 𝘮𝘪𝘵𝘰𝘤𝘩𝘰𝘯𝘥𝘳𝘪𝘢𝘭 𝘳𝘦𝘴𝘱𝘪𝘳𝘢𝘵𝘪𝘰𝘯.

·biorxiv.org·
Cell invasive amyloid assemblies from SARS-CoV-2 peptides can form multiple polymorphs with varying neurotoxicity
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure | PLOS Pathogens
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure | PLOS Pathogens
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure
·journals.plos.org·
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure | PLOS Pathogens
Severe acute respiratory syndrome coronavirus 2 infection leads to Tau pathological signature in neurons
Severe acute respiratory syndrome coronavirus 2 infection leads to Tau pathological signature in neurons
“It is now evident that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection results in a wide range of long-term neurological symptoms and is worryingly associated with the aggravation of Alzheimer’s disease. Little is known about the molecular basis of these manifestations.”
·academic.oup.com·
Severe acute respiratory syndrome coronavirus 2 infection leads to Tau pathological signature in neurons
Google Scholar
Google Scholar
importance of neuropsychology in the early rehabilitation of patients with critical illness after acute COVID infection
·scholar.google.com·
Google Scholar
Google Scholar
Google Scholar
Neurological damages in COVID‐19 patients: Mechanisms and preventive interventions
·scholar.google.com·
Google Scholar
Brain Pathology in COVID-19: Clinical Manifestations and Potential Mechanisms
Brain Pathology in COVID-19: Clinical Manifestations and Potential Mechanisms

Even though Omicron caused less severe disease than Delta, the incidence of neurological manifestations is similar. More than 30% of patients experienced 'brain fog', delirium, stroke, and cognitive impairment, and over half of these patients presented abnormal neuroimaging outcomes.. The most frequent imaging features (affecting >60% of patients) include ischemic infarcts, intracerebral hemorrhages, perfusion abnormalities, and leptomeningeal enhancement. Hypometabolism in the pons, cerebellum, bilateral insula, bilateral medial lobes, and prefrontal cortex indicates brain function dysregulation in COVID patients. The high incidence of cerebrovascular events such as ischemic stroke and intracerebral hemorrhage, indicates potential endothelial injury and coagulation dysfunction. Other investigations have also reported hypoxic alterations in the cerebellum and cerebrum, metabolic alterations of astrocytes, microglial activation, neuro-axonal damage, and neuronal loss.."

·link.springer.com·
Brain Pathology in COVID-19: Clinical Manifestations and Potential Mechanisms
Wes Wilson on Twitter
Wes Wilson on Twitter

Study from CAMH found, via PET scans, elevated levels of the protein TSPO, a brain marker of inflammation, in patients with onset of depression in long covid

more than 200 million globally may experience lingering neurological symptoms from COVID, including depression, memory impairment, slower motor control, low motivation and energy, for months to even years due to brain inflammation from long COVID

this along side everything we have learned in the last 2.5 years ( much summarized in the lit review done by Stanford and Yale, linked in the comments ) moves us a step closer in understanding the underlying biological mechanisms behind these symptoms

·twitter.com·
Wes Wilson on Twitter