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  Resting-state EEG signatures of Alzheimer's disease are driven by periodic but not aperiodic changes

Kopčanová, M., Tait, L., Donoghue, T., Stothart, G., Smith, L., Flores-Sandoval, A., et al. (2024). Resting-state EEG signatures of Alzheimer's disease are driven by periodic but not aperiodic changes. Neurobiology of Disease, 190: 106380. doi:10.1016/j.nbd.2023.106380.

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 Creators:
Kopčanová, Martina1, Author
Tait, Luke2, 3, Author
Donoghue, Thomas4, Author
Stothart, George5, Author
Smith, Laura6, Author
Flores-Sandoval, Aimee7, 8, Author           
Davila-Perez, Paula9, 10, Author
Buss, Stephanie11, 12, Author
Shafi, Mouhsin M.11, 12, Author
Pascual-Leone, Alvaro12, 13, Author
Fried, Peter J.11, 12, Author
Benwell, Christopher S. Y.1, Author
Affiliations:
1Division of Psychology, School of Humanities, Social Sciences and Law, University of Dundee, United Kingdom, ou_persistent22              
2Centre for Systems Modelling and Quantitative Biomedicine, University of Birmingham, United Kingdom, ou_persistent22              
3Cardiff University Brain Research Imaging Centre, United Kingdom, ou_persistent22              
4Department of Biomedical Engineering, Columbia University in the City of New York, NY, USA, ou_persistent22              
5Department of Psychology, University of Bath, United Kingdom, ou_persistent22              
6Wolfson Institute of Population Health (WIPH), Queen Mary University of London, United Kingdom, ou_persistent22              
7Einstein Center for Neurosciences Berlin (ECN), Charité University Medicine Berlin, Germany, ou_persistent22              
8Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society, ou_634549              
9Department of Clinical Neurophysiology, Hospital Universitario Rey Juan Carlos, Móstoles, Spain, ou_persistent22              
10Health Research Institute-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid, Spain, ou_persistent22              
11Department of Neurology, Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA, ou_persistent22              
12Department of Neurology, Harvard Medical School, Boston, MA, USA, ou_persistent22              
13Hinda and Arthur Marcus Institute for Aging Research and Deanna and Sidney Wolk Center for Memory Health, Hebrew SeniorLife, Boston, MA, USA, ou_persistent22              

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Free keywords: Alzheimer's; Dementia; EEG; Oscillations
 Abstract: Electroencephalography (EEG) has shown potential for identifying early-stage biomarkers of neurocognitive dysfunction associated with dementia due to Alzheimer’s disease (AD). A large body of evidence shows that, compared to healthy controls (HC), AD is associated with power increases in lower EEG frequencies (delta and theta) and decreases in higher frequencies (alpha and beta), together with slowing of the peak alpha frequency. However, the pathophysiological processes underlying these changes remain unclear. For instance, recent studies have shown that apparent shifts in EEG power from high to low frequencies can be driven either by frequency specific periodic power changes or rather by non-oscillatory (aperiodic) changes in the underlying 1/f slope of the power spectrum. Hence, to clarify the mechanism(s) underlying the EEG alterations associated with AD, it is necessary to account for both periodic and aperiodic characteristics of the EEG signal. Across two independent datasets, we examined whether resting-state EEG changes linked to AD reflect true oscillatory (periodic) changes, changes in the aperiodic (non-oscillatory) signal, or a combination of both. We found strong evidence that the alterations are purely periodic in nature, with decreases in oscillatory power at alpha and beta frequencies (AD < HC) leading to lower (alpha + beta) / (delta + theta) power ratios in AD. Aperiodic EEG features did not differ between AD and HC. By replicating the findings in two cohorts, we provide robust evidence for purely oscillatory pathophysiology in AD and against aperiodic EEG changes. We therefore clarify the alterations underlying the neural dynamics in AD and emphasise the robustness of oscillatory AD signatures, which may further be used as potential prognostic or interventional targets in future clinical investigations.

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Language(s): eng - English
 Dates: 2023-11-302023-07-132023-12-132023-12-172024-01
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.1016/j.nbd.2023.106380
Other: epub 2023
PMID: 38114048
 Degree: -

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Project name : -
Grant ID : VAC010474
Funding program : -
Funding organization : The Carnegie Trust for The Universities of Scotland
Project name : -
Grant ID : SRG19/191169
Funding program : -
Funding organization : British Academy/Leverhulme Trust and the United Kingdom Department for Business, Energy, and Industrial Strategy
Project name : -
Grant ID : 1K23AG068384-01A1; NIA P01AG031720-8405; R01AG076708; R03AG072233; NIH-NINDS R21NS082870; NIH-NIMH R01MH115949-S1; NIH-NIA R21AG051846; NIA R01AG060987
Funding program : -
Funding organization : National Institutes of Health (NIH)
Project name : -
Grant ID : 2019-AACSF-643094
Funding program : -
Funding organization : Alzheimer's Association
Project name : -
Grant ID : -
Funding program : -
Funding organization : BrightFocus Foundation

Source 1

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Title: Neurobiology of Disease
  Other : Neurobiol. Dis.
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: Oxford : Academic Press
Pages: - Volume / Issue: 190 Sequence Number: 106380 Start / End Page: - Identifier: ISSN: 0969-9961
CoNE: https://pure.mpg.de/cone/journals/resource/954922649144