Abstract

Cerebral amyloidosis is a condition in which β-Amyloid (Aβ) proteins are deposited in the cerebral cortex and is a predictor of Alzheimer’s disease (AD). In the Aging Brain Study, we reported an association between LDL cholesterol and cerebral amyloidosis assessed using PET PiB imaging. LDL comprises multiple species of varying size, density and protein composition, including very large LDL-I which is enriched in ApoE and can bind to ApoE receptors. In this study, LDL particle fractions were measured in plasma samples of 58 participants (40 women and 18 men) of the Aging Brain study. Cerebral amyloidosis was assessed using Pittsburgh Compound B index-Positron Emission Tomography (PiB-PET) imaging. LDL subfractions were analyzed by the method of ion mobility. The subjects were divided into three groups based on PiB tertiles. Compared to the first tertile, total plasma cholesterol as well as LDL cholesterol were greater in patients in the second and third PiB index tertiles (p values = 0.05 and 0.03 respectively). Amongst the LDL subfractions, levels of LDL-I as well as very small LDL-IVa particles were significantly greater in the second and third PiB index tertiles and independent of LDL cholesterol levels (p values = 0.03 and 0.04 respectively). A significant inverse association was also observed between LDL-I and hippocampal volumes (r=-0.33, p=0.02). We suggest that LDL-I level may be a mechanistic biomarker for extent of cerebral amyloidosis. Lipoprotein receptors, particularly LRP-1, participate in Aβ clearance from the brain and its hepatic degradation. One potential mechanism for our findings is competition between plasma-derived LDL-I and brain Aβ that may retard Aβ clearance and degradation.

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