Abstract

AbstractBackgroundThe relationship between metabolic syndrome (MetS) and Alzheimer’s disease (AD) is not fully understood. As Amyloid‐β (Aβ) deposition in the brain is a main pathophysiology of AD and plasma Aβ is closely related to Aβ deposition in the brain, in present study, we investigated the relationship between plasma Aβ and MetS in community population.MethodThis was a population‐based cross‐sectional study. A total of 1275 participants from a village in the suburbs of Xi’an, China were enrolled from October 2014 to March 2015. Fasting venous blood was taken in the morning and plasma Aβ levels were measured by ELISA. The ApoE genotype was detected using polymerase chain reaction and Sanger sequencing. Metabolic syndrome was diagnosed according to ATP‐III riteria, and MetS severity z scores (MetS‐Z) were calculated from waist circumference, triglycerides, HDL cholesterol, systolic blood pressure, and fasting glucose. Relationships between plasma Aβ and MetS were determined using multiple linear regressions.ResultIn the total population and the ApoE ε4 non‐carriers, MetS was associated with higher plasma Aβ40 level (51.704±8.594 pg/ml vs. 53.536±8.063pg/ml, p=0.002;51.693±8.626 pg/ml vs. 53.593±7.990 pg/ml, p=0.003) and lower Aβ42/ Aβ40 ratio(0.814±0.189 vs 0.784±0.170, p=0.018;0.813±0.189 vs. 0.778±0.172, p=0.011). In the multivariable regression analysis, plasma Aβ40 was associated with MetS in the total population and ApoE ε4 non‐carriers (β=1.711, p=0.008; β=1.661, p=0.019) and Aβ42/ Aβ40 ratio (β=‐0.031, p=0.030; β=‐0.035, p=0.024). Furthermore, plasma Aβ40 correlated positively with MetS‐Z in the total population (r=0.073, p=0.009) and the ApoE ε4 non‐carriers (r=0.074, p=0.015), while Aβ42/Aβ40 ratio was negatively related with MetS (r=‐0.064, p=0.038) in ApoE ε4 non‐carriers, but not in ApoE ε4 carriers. There was no significant correlation between MetS and plasma Aβ42.ConclusionMetabolic syndrome was associated with higher plasma Aβ40 level and lower Aβ42/ Aβ40 ratio in ApoE ε4 non‐carriers, but not in ApoE ε4 carriers. This indicated that the relationships between MetS and plasma Aβ may be confounded by ApoE ε4 status.

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