Decreased Global EEG Synchronization in Amyloid Positive Mild Cognitive Impairment and Alzheimer's Disease Patients-Relationship to APOE ε4

The apolipoprotein E (APOE) epsilon 4 allele is a risk factor for Alzheimer's disease (AD) that has been linked to changes in brain structure and function as well as to different biological subtypes of the disease. The present study aimed to investigate the association of APOE epsilon 4 genotypes with brain functional impairment, as assessed by quantitative EEG (qEEG) in patients on the AD continuum. The study population included 101 amyloid positive patients diagnosed with mild cognitive impairment (MCI) (n = 50) and AD (n = 51) that underwent resting-state EEG recording and CSF A beta 42 analysis. In total, 31 patients were APOE epsilon 4 non-carriers, 42 were carriers of one, and 28 were carriers of two APOE epsilon 4 alleles. Quantitative EEG analysis included computation of the global field power (GFP) and global field synchronization (GFS) in conventional frequency bands. Amyloid positive patients who were carriers of APOE epsilon 4 allele(s) had significantly higher GFP beta and significantly lower GFS in theta and beta bands compared to APOE epsilon 4 non-carriers. Increased global EEG power in beta band in APOE epsilon 4 carriers may represent a brain functional compensatory mechanism that offsets global EEG slowing in AD patients. Our findings suggest that decreased EEG measures of global synchronization in theta and beta bands reflect brain functional deficits related to the APOE epsilon 4 genotype in patients that are on a biomarker-verified AD continuum.

Automated summary

The study found that carriers of the APOE ε 4 allele exhibit increased global EEG power in the beta band and decreased global synchronization in theta and beta bands. These EEG characteristics may represent a compensatory mechanism for brain function in APOE ε 4 carriers with AD. The findings suggest that decreased EEG measures of global synchronization in theta and beta bands are indicative of brain functional deficits related to the APOE ε 4 genotype in patients on a biomarker-verified AD continuum.