Dysregulated Levels of Circulating Autoantibodies against Neuronal and Nervous System Autoantigens in COVID-19 Patients.
Level 4 - case-series / case-control
Cross-sectional case-control study comparing circulating autoantibody profiles between COVID-19 patients and healthy controls
PubMed 36832180 · doi:10.3390/diagnostics13040687
What was done
This cross-sectional study measured circulating autoantibodies against a broad panel of neuronal and central nervous system autoantigens (including acetylcholine receptor, glutamate receptor, amyloid-β, α-synuclein, dopamine D1 and D2 receptors, tau, GAD-65, NMDA receptor, BDNF, myelin basic protein, myelin oligodendrocyte glycoprotein, S100-B, GFAP, and enteric nerve) using ELISA. Autoantibody titers were compared between 169 COVID-19 patients (stratified by acute severity: mild [n = 74], severe [n = 65], requiring supplemental oxygen [n = 32]) and 77 healthy controls.
What was found
The abstract reports directional antibody changes without quantitative titers, fold-changes, or p-values. COVID-19 patients exhibited autoantibody dysregulation that correlated with disease severity, including IgG targeting dopamine D1 receptor, NMDA receptor, BDNF, and myelin oligodendrocyte glycoprotein. Compared with healthy controls, COVID-19 patients had elevated IgA autoantibodies against amyloid-β, acetylcholine receptor, dopamine D2 receptor, myelin basic protein, and α-synuclein. Conversely, COVID-19 patients had lower IgA against NMDA receptors and lower IgG against GAD-65, amyloid-β, tau, enteric nerve, and S100-B compared to healthy controls.
Why it matters
The findings demonstrate broad humoral autoantibody perturbation against nervous system targets during and after SARS-CoV-2 infection. This provides plausible autoimmune pathways to investigate for persistent neurological and cognitive symptoms in long COVID syndrome.
Limits
The abstract provides no absolute antibody concentrations, effect sizes, or p-values. The cross-sectional design cannot determine whether autoantibodies pre-existed infection, are temporary epiphenomena of systemic inflammation, or causally drive neurological pathology. Clinical neurological status, symptom persistence, and longitudinal outcomes were not reported.
Cited by
- supports Dr. Aristo Vojdani developed the antibody assays used by Cyrex Laboratories.