Quantitative EEG during memory testing indicates pre‐symptomatic Alzheimer's disease and correlation with MRI

Abstract

Background and ObjectivesIncreasing attention for Alzheimer's disease (AD) have been focused on pre‐symptomatic stage for potential effective treatment. We aim to explore the quantitative electroencephalography (qEEG) during memory testing and evaluate qEEG correlations with MRI volumetric data to investigate the underlying events of pre‐symptomatic AD.MethodsWe employed qEEG test to investigate brain activity during working memory processing (N‐back) in a pre‐symptomatic AD study. Study participants, age 60–100 years, with normal cognition were recruited from the local community, consisting of two subdivisions from cerebrospinal fluid proteins: cognitively healthy with normal amyloid/tau ratio (CH‐NAT, n=10) or pathological amyloid/tau ratio (CH‐PAT, n=14). Behavioral performance and spectral power from 21 recording head sensors were collected during testing. EEG signal (ir)regularity or “noise” levels were measured by spectral entropy (SE). To assess brain anatomical structures, MRI was collected from the same individuals. We analyzed the EEG data for all channels, and explored the spectral power correlations with MRI total gray matter and hippocampal volumes.Results & DiscussionThe behavioral performance was similar between the two groups during lower memory load, and CH‐PATs had significantly less accuracy of performance than CH‐NATs during higher memory load. The qEEG from several sensors were significantly different (p<0.01) between CH‐NAT and CH‐PAT groups during the lower load memory testing when behavioral performances did not differ. The CH‐PAT brain signals were “noisier” compared to CH‐NATs. We interpret the altered brain activity in the CH‐PAT group to indicate a compensation mechanism for the CH‐PATs. qEEG measures from specific sensors correlated with total gray matter volume (p<0.001) and hippocampal volumes (p<0.001); these unexpected results suggest neuroplasticity occurs in the pre‐symptomatic AD stage to compensate for reduction in brain regional volumes. We propose that intervention at the pre‐symptomatic phase of AD using strategies that improve cognitive efficiency may attenuate neurodegeneration.Support or Funding InformationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.