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Research Paper|Volume 12, Issue 6|pp 4945—4952

Fasting blood glucose and cerebrospinal fluid Alzheimer’s biomarkers in non-diabetic cognitively normal elders: the CABLE study

Ya-Nan Ou1, Xue-Ning Shen2, He-Ying Hu1, Hao Hu1, Zuo-Teng Wang1, Wei Xu1, Qiang Dong2, Lan Tan1, Jin-Tai Yu2
  • 1Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
  • 2Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
Received: December 6, 2019Accepted: March 3, 2020Published: March 17, 2020
https://doi.org/10.18632/aging.102921

Copyright © 2020 Ou et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

It is unclear how blood glucose levels mediate the pathology of Alzheimer's disease (AD). This study aimed to investigate whether fasting blood glucose (FBG) levels are associated with cerebrospinal fluid (CSF) biomarkers preferentially affected by AD in non-diabetic cognitively normal elders. A total of 499 non-diabetic cognitively normal elders were from the Chinese Alzheimer’s Biomarker and LifestyLE (CABLE) study. We detected the associations of FBG with individual CSF measures using multiple linear regression models controlling for age, sex, educational level, and apolipoprotein E (APOE) ε4 genotype. Fasting blood glucose level was positively correlated with CSF Aβ42 level (β = 0.045, p = 0.010), CSF Aβ42/Aβ40 ratio (β = 0.005, p < 0.001), Aβ42/P-tau ratio (β = 0.282, p = 0.013), and Aβ42/T-tau ratio (β = 0.050, p = 0.040). Interaction analysis indicated that gender affected the correlations of FBG level with CSF Aβ40 (p < 0.001) and Aβ42/Aβ40 ratio (p < 0.001). This study raises additional questions about the role of blood glucose in the predisposition to AD and supports the possibility of targeting these processes in pre-symptomatic AD trials in non-diabetic elders.