Please use this identifier to cite or link to this item:
https://hdl.handle.net/20.500.14365/5532
Title: | Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia | Authors: | Jiang, Yang Neal, Jennifer Sompol, Pradoldej Yener, Görsev Arakaki, Xianghong Norris, Christopher M. Farina, Francesca R. |
Keywords: | ACE2 Alzheimer's disease and related dementia astrocytes background frequency brain fog coronavirus and EEG COVID-19 encephalopathy inflammatory cytokine storm Long COVID long COVID resting EEG SARS-CoV-2 Cognitive Impairment Mouse Model Brain Eeg Hypoxia Astrocytes Sars-Cov-2 Electroencephalogram Calcineurin Dysfunction |
Publisher: | WILEY | Abstract: | Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting brain fog and mild cognitive impairments even months after the acute phase of infection. Resting-state EEG abnormalities include EEG slowing (reduced alpha rhythm; increased slow waves) and epileptiform activity. An expert panel conducted a systematic review to present compelling evidence that cognitive deficits due to COVID-19 and to Alzheimer's disease and related dementia (ADRD) are driven by overlapping pathologies and neurophysiological abnormalities. EEG abnormalities seen in COVID-19 patients resemble those observed in early stages of neurodegenerative diseases, particularly ADRD. It is proposed that similar EEG abnormalities in Long COVID and ADRD are due to parallel neuroinflammation, astrocyte reactivity, hypoxia, and neurovascular injury. These neurophysiological abnormalities underpinning cognitive decline in COVID-19 can be detected by routine EEG exams. Future research will explore the value of EEG monitoring of COVID-19 patients for predicting long-term outcomes and monitoring efficacy of therapeutic interventions. Highlights Abnormal intrinsic electrophysiological brain activity, such as slowing of EEG, reduced alpha wave, and epileptiform are characteristic findings in COVID-19 patients. EEG abnormalities have the potential as neural biomarkers to identify neurological complications at the early stage of the disease, to assist clinical assessment, and to assess cognitive decline risk in Long COVID patients. Similar slowing of intrinsic brain activity to that of COVID-19 patients is typically seen in patients with mild cognitive impairments, ADRD. Evidence presented supports the idea that cognitive deficits in Long COVID and ADRD are driven by overlapping neurophysiological abnormalities resulting, at least in part, from neuroinflammatory mechanisms and astrocyte reactivity. Identifying common biological mechanisms in Long COVID-19 and ADRD can highlight critical pathologies underlying brain disorders and cognitive decline. It elucidates research questions regarding cognitive EEG and mild cognitive impairment in Long COVID that have not yet been adequately investigated. | URI: | https://doi.org/10.1002/alz.14089 https://hdl.handle.net/20.500.14365/5532 |
ISSN: | 1552-5260 1552-5279 |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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