TY  - JOUR
AV  - public
IS  - 2
KW  - EEG
KW  -  alpha
KW  -  amyloid
KW  -  neurodegeneration
KW  -  tau
N2  - Electroencephalography signatures of amyloid-?, 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-? 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 A?42/40 ratio (r2 = 0.270; P?=?0.003), phosphoTau (pTau181, r2 = 0.290; P?=?0.001) and pTau181/A?42 (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.
A1  - Tanabe, S
A1  - Bo, A
A1  - White, M
A1  - Parker, M
A1  - Farahbakhsh, Z
A1  - Ballweg, T
A1  - Casey, C
A1  - Betthauser, T
A1  - Zetterberg, H
A1  - Blennow, K
A1  - Christian, B
A1  - Bendlin, BB
A1  - Johnson, S
A1  - Sanders, RD
VL  - 2
JF  - Brain Communications
N1  - 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
TI  - Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology
UR  - https://doi.org/10.1093/braincomms/fcaa099
Y1  - 2020/07/15/
ID  - discovery10111044
ER  -