Just a layperson, but this paper seems to make unsupported leaps, and fails my sniff test. For example: > In addition to respiratory and cardiac manifestations

Just a layperson, but this paper seems to make unsupported leaps, and fails my sniff test. For example: > In addition to respiratory and cardiac manifestations, it has been reported that approximately one-third of patients with COVID-19 develop neurological symptoms, including headache, disturbed consciousness, and paresthesias. Headache can be caused by sinus infections! Covid infects the sinuses. Disturbed consciousness can be caused by fever or sickness behavior. Paresthesias (e.g. feeling your skin crawl) are also non-specific. They're neurologic symptoms in a technically correct but meaningless sense. There's also only 11 patients - dead patients - in the study, with an average age of 70. I couldn't tell clearly what the control group was, other than "healthy." Did the control group never have covid? Did they recover and die of unrelated issues? The 11 patients succumbed to COVID itself - there's nothing in this article other than analogies and "might be"s to suggest these phenotypical changes last after acute infection. Finally, they hypothesize that covid may cause tau hyperphosphorylation by leaking through the blood-brain barrier. The BBB gets leaky in older patients, I see nothing to suggest COVID makes it leaky, so nothing suggests that explains long COVID in younger patients. They end with a scary hypothesis that long covid is the prodromal state of an Alzheimer's-like dementia, but long COVID is most similar to CFS/ME, and we'd know by now if CFS patients slip into dementia - they don't. I think this is a paper by Alzheimer's researchers about a hot topic, grasping at straws and fearmongering.