A study of alpha desynchronization, heart rate, and MRI during stroop testing unmasks pre‐symptomatic Alzheimer's disease

Abstract

Background. Alzheimer's disease (AD) studies suggested the need to detect pre‐symptomatic stage, when cognitive challenges reveal changes of alpha power (brain hyperactivity). Heart rate (HR) regulates brain oxygen supply, is regulated by the brain (eg. hippocampus and amygdala), and correlated with resting state alpha power. We aimed to compare alpha power, HR, and hippocampal and amygdala volume between pre‐symptomatic AD and normal, aging individuals. Method. We employed quantitative electroencephalography (qEEG) to monitor brain activity during resting and during Stroop interference testing. Cognitively healthy (CH) study participants (demographically matched) were recruited from the local community, consisting of two subgroups based on cerebrospinal fluid (CSF) proteins: with normal amyloid/tau ratio (CH‐NAT, n=20) or pathological amyloid/tau ratio (CH‐PAT, equals pre‐symptomatic AD, n=21). Cognition was assessed using Montreal Cognitive Assessment (MoCA) and Mini‐Mental State Examination‐7 (MMSE‐7). Participants were presented a series of colored words and asked to respond to each word for the color of the ink, including low load (congruent trials, when color matches the word) and high load (incongruent trials, when color does not match the word). Comparisons between two groups include: alpha desynchronization and alpha spectral entropy (SE), as well as the relationships of alpha desynchronization, HR after Stroop testing, and hippocampal and amygdala volumes (1.5T MRI, demographically balanced subgroups). Result. No alpha differences were found during the resting state. Occipital alpha desynchronization of CH‐PATs was more negative than in that of CH‐NATs (p=0.024) during the congruent trials (Figure 1), indicating hyperactivity during low load. CH‐PATs had higher alpha SE during congruent trials (p=0.042 frontal, p=0.039 occipital), and lower frontal SE change from congruent to incongruent trials (p=0.012) (Figure 2), supporting reduced functional reserve. Alpha desynchronization positively correlated with HR in CH‐PATs but not CH‐NATs; alpha desynchronization correlated with hippocampal or amygdala differently between CH‐NATs and CH‐PATs (Figure 4). Multiple spectral frequencies revealed correlations in MMSE‐7 & MoCA that differed between CH‐NATs and CH‐PATs. Conclusion. These results suggest that hyper‐excitability during low load challenge and limited brain reserve is manifest with increasing interference load in pre‐symptomatic AD. We also find brain‐heart coupling is altered in pre‐symptomatic AD.

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