To investigate whether acute SARS‐CoV‐2 infection was associated with (1) amyloidogenic, aggregation‐prone forms of αSyn in the cerebrospinal fluid (CSF), (2) signature of pathogenic changes, and (3) future risk for frank synucleinopathy, the research team compared CSF biomarkers obtained through lumbar puncture for the evaluation of neurologic symptoms from 12 adult patients hospitalized at NYU Langone Health and 20 COVID‐19‐negative neurological controls with a range of neurological pathologies (proxies for central nervous system inflammation).

The COVID-19-positive patients had the following comorbid diagnoses: bilateral interstitial pneumonia with acute hypoxic respiratory failure requiring intubation, mechanical ventilation, and intensive care (n = 4); acute inflammatory demyelinating polyneuropathy (n = 3); and/or encephalopathy at presentation or during hospitalization (n = 7). The COVID-19-negative control group had diagnoses of epilepsy of unknown origin, antibody-associated autoimmune encephalitis, or status epilepticus of various causes (i.e., drug intoxication, intracerebral hemorrhage, hyperammonemia, prior ischemic injury, hydrocephalus). All patients were screened for aggregation‐prone αSyn forms by αSyn seed amplification assays (i.e., αSyn‐SAA, also known as RT‐QuIC or PMCA) performed by Amprion Clinical Laboratory.