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Understanding early Alzheimer's disease pathology by combining neurochemicals with EEG
Author(s) -
Leong Vincent,
Harrington Michael G,
Fonteh Alfred N.,
Arakaki Xianghong
Publication year - 2021
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.057486
Subject(s) - neurochemical , electroencephalography , alpha (finance) , psychology , neuroscience , stroop effect , pathological , medicine , developmental psychology , cognition , construct validity , psychometrics
Background The association between neurochemical pathways and Electroencephalogram (EEG) signals has not been fully explored. We previously showed alpha desynchronization during interference testing decreased in preclinical Alzheimer’s disease. We aim to explore how neurochemical dysfunction corresponds to alpha desynchronization. Method Elderly participants were classified clinically as cognitively healthy (CH, n=14) using the Uniform Data System‐3. Cerebrospinal fluid amyloid ß 42 and tau levels were measured by immunoassays, and CH was subdivided into participants with normal Ab 42 /tau (CH‐NAT, n=6) or pathological Ab 42 /tau (CH‐PAT, n=8). Plasma neurotransmitters and amino levels were measured using a LC/MS method. EEG was recorded during Stroop interference testing for alpha desynchronization (reflect brain activities), where participants were asked to respond to each colored word for the color of the ink, when color and word matches (congruent) or does not match (incongruent). We compared the relationships of alpha desynchronization at brain regions (frontal‐F, central‐C, parietal‐P, left temporal‐LT, right temporal‐RT, occipital‐O) and neurochemicals between the two groups. Result Plasma diaminobutyric acid (DABA) levels negatively correlated with alpha desynchronization in CH‐NAT (FCP: r=‐0.98∼‐0.88, p=0.005∼0.049) but not in CH‐PATs. Similarly, plasma melatonin negatively correlated with alpha desynchronization during congruent trials in CH‐NAT (P: r=‐1, p=0.003) but not in CH‐PATs. For incongruent trials, citrulline levels positively correlated with EEG recordings in CH‐NATs (C,LT: r=0.86∼0.92, p=0.013∼0.003), while an opposite trend was observed in CH‐PATs (r=‐0.69∼‐0.78, p=0.057∼0.022). Glutamine and histidine negatively correlated with alpha desynchronization during incongruent recordings in the CH‐NAT but not in CH‐PAT state. Plasma adrenaline positively correlated with alpha desynchronization during incongruent recordings in the CH‐NAT (C,LT) but not in CH‐PATs. Homocysteine levels negatively correlated with alpha power in CH‐PATs (F,C,P,RT: r=‐0.84∼‐0.74, p=0.010∼0.034), but not in CH‐NATs. Conclusion Our exploratory studies show different association of plasma neurochemical levels with alpha desynchronization. The most significant changes for our small sample size were observed for neurotransmitter metabolites (DABA, glutamine, adrenaline) and antioxidants (homocysteine). Validation of these data using a larger sample size is ongoing. These studies will provide a rationale for modulating neurochemical plasma levels to prevent early AD cognitive deficits and motivate EEG use to monitor the efficacy of these early interventions.