Mohamed, Mohamed S, Johansson, Anton, Jonsson, Jörgen et al. · International journal of molecular sciences · 2022 · DOI
This study reviews how the virus that causes COVID-19 may damage the nervous system and brain, leading to long-term symptoms similar to those seen in other coronavirus outbreaks. The authors identify specific brain mechanisms—involving inflammation, nerve cell communication problems, and hormone regulation—that could explain why some people develop persistent neurological symptoms after COVID-19. These findings suggest potential targets for future treatments.
For ME/CFS patients, understanding molecular mechanisms of post-viral neurological dysfunction is crucial since ME/CFS shares phenotypic overlap with PCS and may involve similar pathogenic pathways. This work identifies specific molecular targets (EAAT2, NMDA receptors, NF-κB signaling) that could be pharmacologically modulated, potentially opening new therapeutic avenues for both post-COVID patients and those with ME/CFS.
This review does not provide direct experimental evidence that these mechanisms are definitively active in PCS patients; it identifies plausible pathways that warrant investigation. The study does not establish causation or quantify the contribution of each proposed mechanism to symptom severity. It also does not directly test whether these mechanisms apply equally to ME/CFS or are unique to post-COVID syndromes.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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