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Brain fog in long COVID: A glutamatergic hypothesis with astrocyte dysfunction accounting for brain PET glucose hypometabolism

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  • Additional Information
    • Contributors:
      Centre Européen de Recherche en Imagerie médicale (CERIMED); Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-École Centrale de Marseille (ECM)-Institut Paoli-Calmettes (IPC); Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Centre National de la Recherche Scientifique (CNRS); Ischémie reperfusion, métabolisme et inflammation stérile en transplantation U 1313 (IRMETIST Poitiers ); Université de Poitiers = University of Poitiers (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM); Universidade Federal do Rio Grande do Sul Porto Alegre (UFRGS); McGill University = Université McGill Montréal, Canada; Pontifícia Universidade Católica do Rio Grande do Sul Brasil = Pontifical Catholic University of Rio Grande do Sul Brazil = Université catholique pontificale de Rio Grande do Sul Brésil (PUC-RS); Imagerie MOléculaire pour applications THéranostiques personnalisées (IMOTHEP); Institut FRESNEL (FRESNEL); Aix Marseille Université (AMU)-École Centrale de Marseille (ECM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)-École Centrale de Marseille (ECM)-Centre National de la Recherche Scientifique (CNRS)-Hôpital de la Timone CHU - APHM (TIMONE)
    • Publication Information:
      HAL CCSD
      Elsevier
    • Publication Date:
      2023
    • Collection:
      Université de Poitiers: Publications de nos chercheurs.ses (HAL)
    • Abstract:
      International audience ; Brain [18F]FDG-PET scans have revealed a glucose hypometabolic pattern in patients with long COVID. This hypometabolism might reflect primary astrocyte dysfunction. Astrocytes play a key role in regulating energy metabolism to support neuronal and synaptic activity, especially activity involving glutamate as the main neurotransmitter. Neuroinflammation is one of the purported mechanisms to explain brain damage caused by infection with SARS-CoV-2. Microglial activation can trigger reactive astrogliosis, contributing to neuroinflammatory changes. These changes can disturb glutamatergic homeostasis, ultimately leading to cognitive fatigue, which has been described in other clinical situations. We hypothesize that glutamatergic dysregulation related to astrocyte dysfunction could be the substrate of brain PET hypometabolism in long COVID patients with brain fog. Based on these elements, we propose that therapeutics targeting astrocytic glutamate regulation could help mitigate long COVID neurological manifestations.
    • Relation:
      hal-04406602; https://amu.hal.science/hal-04406602; https://amu.hal.science/hal-04406602/document; https://amu.hal.science/hal-04406602/file/Brain%20fog%20in%20long%20COVID_A%20glutamatergic%20hypothesis%20with%20astrocyte.pdf
    • Accession Number:
      10.1016/j.mehy.2023.111186
    • Online Access:
      https://amu.hal.science/hal-04406602
      https://amu.hal.science/hal-04406602/document
      https://amu.hal.science/hal-04406602/file/Brain%20fog%20in%20long%20COVID_A%20glutamatergic%20hypothesis%20with%20astrocyte.pdf
      https://doi.org/10.1016/j.mehy.2023.111186
    • Rights:
      http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess
    • Accession Number:
      edsbas.CC161F89