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Tytuł pozycji:

Creutzfeldt-Jakob disease in a man with COVID-19: SARS-CoV-2-accelerated neurodegeneration?

Tytuł:
Creutzfeldt-Jakob disease in a man with COVID-19: SARS-CoV-2-accelerated neurodegeneration?
Autorzy:
Young MJ; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, United States. Electronic address: .
O'Hare M; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, United States.
Matiello M; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, United States.
Schmahmann JD; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, United States.
Źródło:
Brain, behavior, and immunity [Brain Behav Immun] 2020 Oct; Vol. 89, pp. 601-603. Date of Electronic Publication: 2020 Jul 15.
Typ publikacji:
Case Reports; Journal Article
Język:
English
Imprint Name(s):
Publication: <2000- > : Amsterdam : Elsevier
Original Publication: San Diego : Academic Press, [c1987-
MeSH Terms:
Brain/*diagnostic imaging
Coronavirus Infections/*complications
Creutzfeldt-Jakob Syndrome/*complications
Pneumonia, Viral/*complications
Aged ; Betacoronavirus ; Brain/physiopathology ; COVID-19 ; Coronavirus Infections/immunology ; Creutzfeldt-Jakob Syndrome/diagnosis ; Creutzfeldt-Jakob Syndrome/immunology ; Creutzfeldt-Jakob Syndrome/physiopathology ; Disease Progression ; Electroencephalography ; Fluorodeoxyglucose F18 ; Humans ; Magnetic Resonance Imaging ; Male ; Pandemics ; Pneumonia, Viral/immunology ; Positron-Emission Tomography ; Radiopharmaceuticals ; SARS-CoV-2
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Contributed Indexing:
Keywords: COVID-19; Neurodegeneration; Prion disease; Psychoneuroimmunology
Substance Nomenclature:
0 (Radiopharmaceuticals)
0Z5B2CJX4D (Fluorodeoxyglucose F18)
Entry Date(s):
Date Created: 20200719 Date Completed: 20201022 Latest Revision: 20201218
Update Code:
20240105
PubMed Central ID:
PMC7362815
DOI:
10.1016/j.bbi.2020.07.007
PMID:
32681865
Czasopismo naukowe
We describe a man whose first manifestations of Creutzfeldt-Jakob disease occurred in tandem with symptomatic onset of coronavirus disease 2019 (COVID-19). Drawing from recent data on prion disease pathogenesis and immune responses to SARS-CoV-2, we hypothesize that the cascade of systemic inflammatory mediators in response to the virus accelerated the pathogenesis of our patient's prion disease. This hypothesis introduces the potential relationship between immune responses to the novel coronavirus and the hastening of preclinical or manifest neurodegenerative disorders. The global prevalence of both COVID-19 and neurodegenerative disorders adds urgency to the study of this potential relationship.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 Elsevier Inc. All rights reserved.)

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