COVID Chronicles
@covidchronicles.bsky.social
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Chronicling my journey through purgatory, graphically. Former athlete/composer/writer/woodworker. Saddled with debilitating COVID-induced metabolic dysfunction since Nov 2022. #LongCOVID #LC #MECFS #PEM #SickJokes
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![As explained in their paper, published in Brain Communications on October 1, 2025, the team hypothesized that patients with brain fog might exhibit disrupted expression of AMPA receptors (AMPARs)—key molecules for memory and learning—based on prior research into psychiatric and neurological disorders such as depression, bipolar disorder, schizophrenia, and dementia. Thus, they used a novel method called [11C]K-2 AMPAR PET imaging to directly visualize and quantify the density of AMPARs in the living human brain.
By comparing imaging data from 30 patients with Long COVID to 80 healthy individuals, the researchers found a notable and widespread increase in the density of AMPARs across the brains of patients. This elevated receptor density was directly correlated with the severity of their cognitive impairment, suggesting a clear link between these molecular changes and the symptoms. Additionally, the concentrations of various inflammatory markers were also correlated with AMPAR levels, indicating a possible interaction between inflammation and receptor expression.
Taken together, the study’s findings represent a crucial step forward in addressing many unresolved issues regarding Long COVID. The systemic increase in AMPARs provides a direct biological explanation for the cognitive symptoms, highlighting a target for potential treatments. For example, drugs that suppress AMPAR activity could be a viable approach to mitigate brain fog. Interestingly, the team’s analysis also demonstrated that imaging data can be used to distinguish patients from healthy controls with 100% sensitivity and 91% specificity. https://scitechdaily.com/scientists-finally-reveal-biological-basis-of-long-covid-brain-fog/](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:z7fq5sb3thfww72ndrnpuivv/bafkreicr5eti35ag3oyopblcr2ljo24ja5a2qi5x6khmxf3pixuer7vgm4@jpeg)
![Cognitive symptoms after Covid-19, the disease caused by SARS-CoV-2, are well-recognized. Whether objectively measurable cognitive deficits exist and how long they persist are unclear.
Of the 141,583 participants who started the online cognitive assessment, 112,964 completed it. In a multiple regression analysis, participants who had recovered from Covid-19 in whom symptoms had resolved in less than 4 weeks or at least 12 weeks had similar small deficits in global cognition as compared with those in the no–Covid-19 group, who had not been infected with SARS-CoV-2 or had unconfirmed infection (−0.23 SD [95% confidence interval {CI}, −0.33 to −0.13] and −0.24 SD [95% CI, −0.36 to −0.12], respectively); larger deficits as compared with the no–Covid-19 group were seen in participants with unresolved persistent symptoms (−0.42 SD; 95% CI, −0.53 to −0.31). Larger deficits were seen in participants who had SARS-CoV-2 infection during periods in which the original virus or the B.1.1.7 variant was predominant than in those infected with later variants (e.g., −0.17 SD for the B.1.1.7 variant vs. the B.1.1.529 variant; 95% CI, −0.20 to −0.13) and in participants who had been hospitalized than in those who had not been hospitalized (e.g., intensive care unit admission, −0.35 SD; 95% CI, −0.49 to −0.20). Results of the analyses were similar to those of propensity-score–matching analyses. In a comparison of the group that had unresolved persistent symptoms with the no–Covid-19 group, memory, reasoning, and executive function tasks were associated with the largest deficits (−0.33 to −0.20 SD); these tasks correlated weakly with recent symptoms, including poor memory and brain fog.
https://www.nejm.org/doi/full/10.1056/NEJMoa2311330#f2](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:z7fq5sb3thfww72ndrnpuivv/bafkreibjcb56wfmiwitovgfhmiasedvg623uxibytjx64kon3qbqexrgsy@jpeg)
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![La densité des AMPAR était significativement élevée dans l'ensemble du cerveau chez les patients atteints de COVID longue cognitive (Cog-LC) par rapport aux témoins sains (HC). L'augmentation systémique de l'expression de l'AMPAR pourrait résulter de mécanismes compensatoires pour la perte inconnue de fonction cérébrale. Cependant, nous avons constaté une corrélation négative significative entre les scores des sous-échelles RBANS, Picture Naming et Figure Recall, et l'absorption de [11C]K-2 dans toutes les régions du cerveau, où l'absorption de [11C]K-2 était plus élevée chez les patients que chez les participants sains. Comme nous n'avons observé aucune corrélation négative significative entre ces sous-échelles RBANS et les échelles dépressives, les troubles cognitifs du Cog-LC n'étaient pas liés à des symptômes dépressifs, mais à une régulation à la hausse des AMPAR après une infection par le SARS-CoV-2. Ces résultats suggèrent qu'une augmentation généralisée de l'expression des AMPAR dans le cerveau représente un état pathologique. Source : Yu Fujimoto et al., Augmentation systémique des récepteurs AMPA associée à des troubles cognitifs liés à la COVID longue, Brain Communications, vol. 7, n° 5, 2025, fcaf337 — https://doi.org/10.1093/braincomms/fcaf337](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:cenpn5mu5fvletfxvroiwmlz/bafkreiabr63dqewgpx3qwben2jffk7rpqoei5bbjaqodig47qfw533yur4@jpeg)
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