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ASSOCIATION BETWEEN SERUM LIPIDS AND CEREBRAL AMYLOIDOSIS IN COGNITIVELY NORMAL ELDERLY

      Background

      Cerebral amyloid-beta protein (Aβ) deposition has been considered as a key initiating step in Alzheimer's disease (AD) process. Although many preclinical studies have suggested the possible linkage between dyslipidemia and cerebral amyloidogenesis or amyloid deposition, the association between serum lipids and cerebral Aβ deposition in human brain is still poorly known. We aimed to investigate such association in cognitively normal (CN) elderly individuals.

      Methods

      Sixty two CN elderly individuals were included. All participants received comprehensive clinical and neuropsychological assessment based on the CERAD protocol, 11 C labeled Pittsburgh Compound B (PiB) positron emission tomography volumetric MRI, and quantification for serum lipid components including total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) with apolipoprotein A1 (APOA1) and B (APOB).

      Results

      Global cerebral Aβ deposition was defined as mean cortical PiB retention of the cortical regions including frontal, lateral temporal, lateral parietal and precuneus/posterior cingulate cortices. Univariate analyses showed significant positive association of mean cortical PiB retention with the levels of serum TG and APOB, and negative association with HDL-C and APOA1 levels. Multivariate statistical models that controlled age, education, gender, apolipoprotein E ε4 genotype revealed independent associations between the levels of TG and mean cortical 11 C-PiB retention. Higher serum TG level was associated with heavier cortical 11 C-PiB retention. No association was found between both total cholesterol and LDL-C, and cortical 11 C-PiB retention.

      Conclusions

      Our findings strongly support the association between lipid profiles in serum, especially TG level, and the degree of cerebral amyloidosis in cognitively normal elderly people.The findings also suggest that the mechanisms through which serum lipid or lipoproteins affect cerebral Aβ could provide novel targets of AD therapeutics. More specifically, various approaches known to reduce blood TG level, such as moderate exercise and omega-3 fatty acid intake, might be helpful for slowing Aβ deposition and reducing AD occurrence.