@article{discovery10111044,
            note = {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},
           title = {Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology},
         journal = {Brain Communications},
          number = {2},
          volume = {2},
           month = {July},
            year = {2020},
             url = {https://doi.org/10.1093/braincomms/fcaa099},
          author = {Tanabe, S and Bo, A and White, M and Parker, M and Farahbakhsh, Z and Ballweg, T and Casey, C and Betthauser, T and Zetterberg, H and Blennow, K and Christian, B and Bendlin, BB and Johnson, S and Sanders, RD},
        abstract = {Electroencephalography signatures of amyloid-{\ensuremath{\beta}}, 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-{\ensuremath{\beta}} 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{\ensuremath{\beta}}42/40 ratio (r2 = 0.270; P = 0.003), phosphoTau (pTau181, r2 = 0.290; P = 0.001) and pTau181/A{\ensuremath{\beta}}42 (r2 = 0.343; P {\ensuremath{<}} 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.},
        keywords = {EEG, alpha, amyloid, neurodegeneration, tau}
}