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Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia
Jiang Y, Neal J, Sompol P, Yener G, Arakaki X, Norris CM, Farina FR, Ibanez A et al.. Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024-08-29
Topic: Amyloid, tau and blood-test diagnosis
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.
Key findings
- 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.
Why it matters
An expert panel reviewed evidence that brain-wave (EEG) changes after COVID-19, such as slowing and a reduced alpha rhythm, resemble those seen in early Alzheimer's disease and related dementias. They propose that both share inflammation, reactive astrocytes (support cells), low oxygen and blood vessel injury. Routine EEG might help flag Long COVID patients at risk of cognitive decline, though the authors say this still needs to be studied.
Study details
- Study designsystematic review
- Participants19
- Evidence strengthHigh
How this study scored 69/100
Published in a leading specialty journal, and it is a systematic review of all the studies on the question. Scored zero for effect reported because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association) |
| Journal's citation record | 2 / 4 | Alzheimer s & Dementia: journal h-index 228 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A systematic review of all the studies on the question |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2024 — within 3 year(s) of the newest study here |
| Sample size | 1 / 4 | 19 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | 3 / 7 | Cited 27 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.8 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 3 / 6 | Cited 6.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 27 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Mihály Hajós: h-index 52 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Yale University: institution h-index 1,927 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 12 institution(s) in 6 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39206795) |
| Free to read | 2 / 2 | Free to read |
| Total | 69 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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APA 7th
Jiang, Y., Neal, J., Sompol, P., Yener, G., Arakaki, X., Norris, C. M., et al. (2024). Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.14089
Vancouver
Jiang Y, Neal J, Sompol P, Yener G, Arakaki X, Norris CM, et al. Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2024. doi:10.1002/alz.14089. PMID: 39206795.
BibTeX
@article{jiang2024-39206795,
author = {Jiang, Y. and Neal, J. and Sompol, P. and Yener, G. and Arakaki, X. and Norris, C. M. and Farina, F. R. and Ibanez, A. and others},
title = {{Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia}},
journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
year = {2024},
doi = {10.1002/alz.14089},
pmid = {39206795},
url = {https://doi.org/10.1002/alz.14089}
}
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