Growing evidence seems to indicate that many patients develop a chronic condition characterised by fatigue and neuropsychiatric symptoms, called long-COVID. Most of the vaccines produced so far for COVID-19 also cause human cells to produce the spike protein.
This scientific article (https://pubmed.ncbi.nlm.nih.gov/35028901/) describes perivascular inflammation in the brains of patients who died with Covid-19, while others have shown that the spike protein could damage the endothelium, resulting in perivascular inflammation. In addition, the spike protein appears to share antigenic epitopes with human molecular chaperones resulting in autoimmunity and may activate toll-like receptors (TLRs), leading to the release of inflammatory cytokines. Furthermore, some antibodies produced against the spike protein (either by disease or vaccination) are non-neutralising. Consequently, the question arises whether the spike protein entering the brain or expressed by brain cells could activate microglia, alone or together with inflammatory cytokines, leading to neuroinflammation and contributing to long-COVID. Thus, there is an urgent need to better understand the neurotoxic effects of the spike protein and to consider possible interventions to mitigate its brain-damaging effects.
