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Diabetes mellitus, HBA1C, and in vivo Alzheimer’s disease pathologies
Author(s) -
Han Dongkyun,
Byun Min Soo,
Yi Dahyun,
Lee Jun Ho,
Byeon Gihwan,
Joung Haejung,
Moon Seok Woo,
Sohn Bo Kyung,
Lee JunYoung,
Kim Yu Kyeong,
Lee YunSang,
Sohn ChulHo,
Lee Dong Young
Publication year - 2020
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.044752
Subject(s) - dementia , glycated hemoglobin , diabetes mellitus , medicine , context (archaeology) , apolipoprotein e , alzheimer's disease , positron emission tomography , disease , endocrinology , psychology , type 2 diabetes , nuclear medicine , biology , paleontology
Background Although previous studies have reported associations of diabetes mellitus (DM) with cognitive impairment or dementia, the exact pathophysiological links underlying the associations remain incompletely understood. In this context, we aimed to investigate the associations of DM or glycated hemoglobin (HbA1c) with in vivo Alzheimer’s disease (AD) pathologies such as cerebral beta‐amyloid protein (Aβ) deposition and tau deposition. Method Total 136 participants (71 cognitively normal, 31 mild cognitive impairment, and 34 AD dementia) from the Korean Brain Aging Study for Early Diagnosis & Prediction of Alzheimer’s Disease (KBASE), an ongoing prospective cohort study, were included for this analysis. All participants underwent comprehensive clinical and neuropsychological assessment, 11 C labelled Pittsburgh Compound B (PiB) positron emission tomography (PET), 11 F AV‐1451 PET, magnetic resonance imaging, apolipoprotein E genotyping, and HbA1c measurement. Result Neither the presence of DM nor HbA1c level was associated with global Aβ deposition after controlling for age, sex, education, vascular risk score (except DM), apolipoprotein e4 positivity, and clinical diagnosis. In contrast, higher HbA1c was significantly associated with lower AD‐signature region tau deposition and the presence of DM showed a trend level association with decreased tau deposition. Additionally, we found significant Aβ deposition x HbA1c (or the presence of DM) interaction effect on tau deposition. While higher Aβ deposition was significantly related to increased tau deposition in lower HbA1c (or DM negative) subgroup, there was no such relationship between Aβ and tau deposition in higher HbA1c (or DM positive) one. Sensitivity analyses including only cognitively normal individuals also showed similar results. Conclusion Our results indicate that DM or higher blood glucose may not contribute to cognitive impairment or dementia via AD‐specific pathologies, especially amyloid deposition. Therefore, other non‐AD pathophysiological contributions including vascular pathologies should be considered. Although being very cautious, high blood glucose may relate to delayed brain tau deposition.