%0 Journal Article
%A Tanabe, S
%A Bo, A
%A White, M
%A Parker, M
%A Farahbakhsh, Z
%A Ballweg, T
%A Casey, C
%A Betthauser, T
%A Zetterberg, H
%A Blennow, K
%A Christian, B
%A Bendlin, BB
%A Johnson, S
%A Sanders, RD
%D 2020
%F discovery:10111044
%J Brain Communications
%K EEG, alpha, amyloid, neurodegeneration, tau
%N 2
%T Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology
%U https://discovery.ucl.ac.uk/id/eprint/10111044/
%V 2
%X Electroencephalography signatures of amyloid-β, tau and neurodegenerative pathologies would aid in screening for, tracking progression of, and critically, understanding the pathogenesis of dementia. We hypothesized that slowing of the alpha peak frequency, as a signature of hyperpolarization-activated cyclic nucleotide gated ‘pacemaker’ channel activity, would correlate with amyloid and tau pathology burden measured by amyloid (Pittsburgh Compound B) and tau (MK-6240) positron emission tomography or CSF biomarkers. We also hypothesized that EEG power would be associated with neurodegeneration (CSF neurofilament light and hippocampal volume). Wakeful high-density EEG data were collected from 53 subjects. Both amyloid-β and tau pathology were associated with slowing in the alpha peak frequency [Pittsburgh Compound B (+) vs. Pittsburgh Compound B (−) subjects, P = 0.039 and MK-6240 (+) vs. MK-6240 (−) subjects, P = 0.019]. Furthermore, slowing in the peak alpha frequency correlated with CSF Aβ42/40 ratio (r2 = 0.270; P = 0.003), phosphoTau (pTau181, r2 = 0.290; P = 0.001) and pTau181/Aβ42 (r2 = 0.343; P < 0.001). Alpha peak frequency was not associated with neurodegeneration. Higher CSF neurofilament light was associated with lower total EEG power (r2 = 0.136; P = 0.018), theta power (r2 = 0.148; P = 0.014) and beta power (r2 = 0.216; P = 0.002); the latter was also associated with normalized hippocampal volume (r2 = 0.196; P = 0.002). Amyloid-tau and neurodegenerative pathologies are associated with distinct electrophysiological signatures that may be useful as mechanistic tools and diagnostic/treatment effect biomarkers in clinical trials.
%Z This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com