Covid and Brain Damage
“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.”
𝘼𝙢𝙮𝙡𝙤𝙞𝙙 𝙖𝙜𝙜𝙧𝙚𝙜𝙖𝙩𝙚𝙨 𝙛𝙧𝙤𝙢 𝙎𝘼𝙍𝙎-𝘾𝙤𝙑-2 𝙥𝙚𝙥𝙩𝙞𝙙𝙚𝙨 𝙧𝙚𝙖𝙙𝙞𝙡𝙮 𝙚𝙣𝙩𝙚𝙧 𝙣𝙚𝙪𝙧𝙤𝙣𝙖𝙡 𝙘𝙚𝙡𝙡𝙨, 𝘢𝘯𝘥 𝘵𝘩𝘪𝘴 𝘤𝘢𝘶𝘴𝘦𝘴 𝘢 𝘳𝘦𝘥𝘶𝘤𝘵𝘪𝘰𝘯 𝘪𝘯 𝘵𝘩𝘦𝘪𝘳 𝘮𝘪𝘵𝘰𝘤𝘩𝘰𝘯𝘥𝘳𝘪𝘢𝘭 𝘳𝘦𝘴𝘱𝘪𝘳𝘢𝘵𝘪𝘰𝘯.
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.."
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
Thread on Twitter: New study documents the case of two previously healthy sisters - 11 and 13-years-old - with new-onset cognitive decline after mild covid. The ability of their brains to consume glucose had been impaired - an initiating factor for dementia, Parkinson's and Alzheimer's disease 🧵
Interesting study: Inflammatory and mental health sequelae of COVID-19
"The COVID-19 pandemic has caused significant negative consequences to mental health. Increased inflammatory factors and neuropsychiatric symptoms, such as cognitive impairment (“brain fog”), depression, and anxiety are associated with long COVID [post-acute sequelae of SARS-CoV-2 infection (PASC), termed neuro-PASC]"
➡️Biomarker: MIG
"Growing evidence supporting the usefulness of circulating MIG(monokine induced by gamma interferon (IFN-γ) aka CXCL9) levels as a biomarker reflecting IFN-γ production, which is important because individuals with neuro-#PASC/ neuro-#Longcovid have elevated IFN-γ responses to internal SARS-CoV-2 proteins"