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Are autoantibodies behind the »brain fog«?

Posted by Otto Knotzer on January 26, 2023 - 8:57am
Cognitive impairments are among the possible long-term consequences of Covid-19. Autoimmune mechanisms in the central nervous system could play a key role in its development, as a pilot study by the Berlin Charité and the University of Cologne suggests. These findings could serve as a starting point for research into immunotherapeutic therapies.
 
Laura Rudolph
01/25/2023 5:00 p.m
 
 
 
 

A research team led by Dr. Christiana Franke from the Berlin Charité . To do this, it analyzed the cerebrospinal fluid, the blood and the cognition of 50 long-Covid patients who stated that they had suffered from cognitive impairment since the corona infection they had undergone . According to the pilot study , antineuronal antibodies in CSF correlate with impaired mental performance. 

"These results indicate that in those affected in whom antineuronal antibodies are detectable, autoimmune mechanisms could contribute to the development of cognitive impairments after Covid-19 ," concludes Franke in a  press release  from the German Society for Neurology . "In these patients with autoantibodies , an immunotherapeutic approach would therefore be justified. However, we do not know at this point in time whether the autoantibodies are the cause of the symptoms or just a side effect.«

Antineuronal antibodies against a variety of epitopes 

The first thing that stood out in the study was that the majority of the participants could not confirm the subjectively perceived cognitive impairment using the Montreal Cognitive Assessment Test (MoCA test). A maximum of 30 points can be achieved in this validated test. A result of 26 points or more is considered normal, smaller values ​​indicate reduced cognition. Only 18 people scored 25 or lower on the MoCA test. The abnormal MoCA test values ​​in the study were significantly associated with the presence of antineuronal antibodies in the CSF.

Antineuronal antibodies were found in 26 study participants (52 percent), including nine patients in serum only, three patients in CSF only, and 14 in both serum and CSF. Among other things, the autoantibodies were directed against myelin, an isoform of glutamate decarboxylase (GAD65), the NMDA receptor and against a large number of undetermined epitopes on brain slices. This was revealed by cell-based assays and indirect immunofluorescence studies on mouse brain slices. 

Further studies are necessary to decipher the causal pathomechanisms, Franke concluded. It is also still unclear whether and which immunotherapies could possibly help those affected who are autoantibody-positive.