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.
Highlights
Mounting evidence supports the notion that type 2 diabetes mellitus (T2DM) could increase the risk of Alzheimer’s disease (AD) [1,2,3] via multiple possible pathways, including cerebrovascular disease and neurodegeneration [2]
This study aimed to investigate whether fasting blood glucose (FBG) levels are associated with cerebrospinal fluid (CSF) biomarkers preferentially affected by Alzheimer's disease (AD) in non-diabetic cognitively normal elders
We discovered that FBG levels were positively associated with CSF Aβ42 levels in cognitively normal elders without T2DM
Summary
Mounting evidence supports the notion that type 2 diabetes mellitus (T2DM) could increase the risk of Alzheimer’s disease (AD) [1,2,3] via multiple possible pathways, including cerebrovascular disease and neurodegeneration [2]. One study suggested that the neurodegenerative effects of T2DM might be driven by pathways that promote neuronal tau more than βamyloid (Aβ) [4]. A previous cohort study among non-diabetic AD patients found that cerebrospinal fluid (CSF)/plasma glucose ratio was inversely related with CSF Aβ42 level rather than CSF tau level [5]. One study indicated that Aβ42 in CSF was positively associated with T2DM status [6]. Elevated fasting serum glucose has been linked to decreased memory functioning in cognitively normal (CN) older adults and may be a risk factor for cognitive impairment or predisposition to AD [8]. AD prevention research may benefit from the research on the association between elevated fasting blood glucose and AD biomarkers in non-diabetic cognitively normal individuals
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