Tanabe, S;
Bo, A;
White, M;
Parker, M;
Farahbakhsh, Z;
Ballweg, T;
Casey, C;
... Sanders, RD; + view all
(2020)
Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology.
Brain Communications
, 2
(2)
, Article fcaa099. 10.1093/braincomms/fcaa099.
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Abstract
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.
| Type: | Article |
|---|---|
| Title: | Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology |
| Location: | England |
| Open access status: | An open access version is available from UCL Discovery |
| DOI: | 10.1093/braincomms/fcaa099 |
| Publisher version: | https://doi.org/10.1093/braincomms/fcaa099 |
| Language: | English |
| Additional information: | 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 |
| Keywords: | EEG, alpha, amyloid, neurodegeneration, tau |
| UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Neurodegenerative Diseases |
| URI: | https://discovery-pp.ucl.ac.uk/id/eprint/10111044 |
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