According to a pilot study, autoantibodies in the CSF, for example against myelin, glutamate decarboxylase or the NMDA receptor, correlate with cognitive losses after a corona infection. / Photo: Getty Images/LightFieldStudios
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.«
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.
