Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology. Issue 2 (15th July 2020)
- Record Type:
- Journal Article
- Title:
- Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology. Issue 2 (15th July 2020)
- Main Title:
- Cohort study of electroencephalography markers of amyloid-tau-neurodegeneration pathology
- Authors:
- Tanabe, Sean
Bo, Amber
White, Marissa
Parker, Margaret
Farahbakhsh, Zahra
Ballweg, Tyler
Casey, Cameron
Betthauser, Tobey
Zetterberg, Henrik
Blennow, Kaj
Christian, Brad
Bendlin, Barbara B
Johnson, Sterling
Sanders, Robert D - Abstract:
- 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 ( r 2 = 0.270; P = 0.003), phosphoTau (pTau181, r 2 = 0.290; P = 0.001) and pTau181 /Aβ42 ( r 2 = 0.343; P < 0.001). Alpha peak frequency was not associated with neurodegeneration. Higher CSF neurofilament light was associated with lower total EEG power ( r 2 = 0.136; P = 0.018), theta power ( r 2 = 0.148; P = 0.014) and beta power ( r 2 = 0.216; P = 0.002); the latter was also associated with normalized hippocampal volume ( r 2 = 0.196; P = 0.002).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 ( r 2 = 0.270; P = 0.003), phosphoTau (pTau181, r 2 = 0.290; P = 0.001) and pTau181 /Aβ42 ( r 2 = 0.343; P < 0.001). Alpha peak frequency was not associated with neurodegeneration. Higher CSF neurofilament light was associated with lower total EEG power ( r 2 = 0.136; P = 0.018), theta power ( r 2 = 0.148; P = 0.014) and beta power ( r 2 = 0.216; P = 0.002); the latter was also associated with normalized hippocampal volume ( r 2 = 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. Abstract : EEG signatures of amyloid-β, tau, and neurodegenerative pathologies would aid in the understanding the pathogenesis of dementia. Both amyloid-β and tau pathology were associated with slowing in the alpha peak frequency while neurodegeneration was associated with lower EEG power. Graphical Abstract: … (more)
- Is Part Of:
- Brain communications. Volume 2:Issue 2(2020)
- Journal:
- Brain communications
- Issue:
- Volume 2:Issue 2(2020)
- Issue Display:
- Volume 2, Issue 2 (2020)
- Year:
- 2020
- Volume:
- 2
- Issue:
- 2
- Issue Sort Value:
- 2020-0002-0002-0000
- Page Start:
- Page End:
- Publication Date:
- 2020-07-15
- Subjects:
- amyloid -- tau -- neurodegeneration -- EEG -- alpha
616 - Journal URLs:
- https://academic.oup.com/braincomms ↗
http://www.oxfordjournals.org/ ↗ - DOI:
- 10.1093/braincomms/fcaa099 ↗
- Languages:
- English
- ISSNs:
- 2632-1297
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 25840.xml