Beyond brain fog: viral proteins as convergent drivers of neuroinflammation and proteinopathy 🚨“COVID-19 never really leaves your brain.” New science review proposes SARSCoV2 viral proteins stay behind as long-lived toxins, triggering chronic neuroinflammation and planting the seeds of Alzheimer’s and Parkinson’s, even after mild infection. This very interesting and eye-catching GERMAN review reframes post-viral neurological syndromes( L0ngC0vid) as driven by persistent viral proteins acting as long-term toxins ("protein-as-pathogen" model), not just the active infection! ➡️Core mechanisms: - SARSCoV2 Spike and OTHER viral proteins activate glial TLR4/TLR2 receptors, triggering chronic neuroinflammatory cascades via NLRP3 inflammasome, - They also disrupt autophagy, allowing toxic protein aggregates (tau, amyloid-beta, α-synuclein) to accumulate and seed neurodegeneration, ➡️SARSCoV2 specific evidence: - Animal studies show Spike protein alone (without live virus) induces TLR4-mediated cognitive deficits, memory impairment, synaptic loss, and sustained neuroinflammation, recapitulating post-COVID syndrome, - Spike binds α-synuclein, accelerating Parkinson-like clumps, ➡️Human data evidence: - Millions experience "brain fog," - Post-COVID patients exhibit measurable brain damage: cortical thinning, hippocampal iron accumulation, and biomarkers of ongoing neuronal injury, ➡️Broader risks: - Even mild infections leave lingering proteins that promote Alzheimer’s and Parkinson’s-like pathology via shared pathways, - Same pathways seen in influenza, dengue, West Nile etc, - Mild infection = no protection, ‼️So, according to this review, the “protein-as-pathogen” model makes it crystal clear: every new SARSCoV2 infection (even mild or asymptomatic) deposits more of these long-lived toxic viral proteins into the brain. They don’t fully clear. They accumulate. Each reinfection reloads the TLR4/TLR2 → NLRP3 inflammasome trigger and further collapses autophagy, speeding up the tau/amyloid/α-synuclein proteinopathy and neurodegeneration. SARS-CoV-2 does not just infect. It weaponizes its own proteins as long-lived intracellular saboteurs. Millions are probably already carrying this hidden payload. This is not brain fog. This is a silent, population-scale reprogramming of human brains toward dementia-like decline. The long-term neurological cost will probably dwarf the acute pandemic itself! #AvoidSars2 #AvoidReinfections sciencedirect.com/science/ar…

Ich hab mit edition a ein Buch über ME/CFS gemacht. Hoffentlich ist es hilfreich vor allem für jene, wo die Diagnose noch unklar ist. Normale medizinische Versorgung kann es jedenfalls nicht ersetzen. Darum geht mein Anteil zu 100% an CS Nordlicht der @CaritasSocialis.

Excited to share our study by @keylas3 et al. on pathological autoantibodies in people with Long COVID. We asked whether IgG in patients with Long COVID bind to human tissues/antigens and cause pathologies when transferred into mice. With @PutrinoLab doi.org/10.1016/j.cell.2026.…

ME/CFS meets Medizin 💜🩺 Ärzt:innen der Allgemeinmedizin sowie der Fachgruppen Neurologie und Psychiatrie wurden bei der ME/CFS-Fortbildung der ÖGAM Vorarlberg erreicht. Danke an ME/CFS-Spezialist @neurostingl für den hochkarätigen Vortrag! #MECFS #ÖGAM #Vorarlberg