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

•A patient whose first manifestations of CJD occurred in tandem with onset of COVID-19 is described.•The inflammatory cascade in COVID-19 is hypothesized to accelerate prion disease pathogenesis.•We explore the potential link between COVID-19 immune responses and hastening of neurodegenerative disor...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2020-10, Vol.89, p.601-603
Main Authors: Young, Michael J., O'Hare, Meabh, Matiello, Marcelo, Schmahmann, Jeremy D.
Format: Article
Language:English
Subjects:
Aged
Betacoronavirus
Brain - diagnostic imaging
Brain - physiopathology
Coronavirus Infections - complications
Coronavirus Infections - immunology
COVID-19
Creutzfeldt-Jakob Syndrome - complications
Creutzfeldt-Jakob Syndrome - diagnosis
Creutzfeldt-Jakob Syndrome - immunology
Creutzfeldt-Jakob Syndrome - physiopathology
Disease Progression
Electroencephalography
Fluorodeoxyglucose F18
Humans
Magnetic Resonance Imaging
Male
Neurodegeneration
Pandemics
Pneumonia, Viral - complications
Pneumonia, Viral - immunology
Positron-Emission Tomography
Prion disease
Psychoneuroimmunology
Radiopharmaceuticals
SARS-CoV-2
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Description
Summary:•A patient whose first manifestations of CJD occurred in tandem with onset of COVID-19 is described.•The inflammatory cascade in COVID-19 is hypothesized to accelerate prion disease pathogenesis.•We explore the potential link between COVID-19 immune responses and hastening of neurodegenerative disorders.•The rising global prevalence of both COVID-19 and neurodegenerative disorders adds urgency to the study of this potential relationship. 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.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2020.07.007