Studies on the effect of the apolipoprotein E genotype on the lipid profile in Alzheimer\u27s disease

Objective: To determine whether Apolipoprotein E4 (Apo E4) gene status or ApoE gene dose affect the lipid profile in AD. Background: Links between hypercholesterolemia and AD development continue to grow. Presently, limited information exists about the influence of the Apo E genotype on the lipid profile characteristics in AD. Methods: We examined the lipid profiles (total cholesterol (TC), high-density lipoprotein (HDL), lower-density lipoprotein (LDL), TC/HDL ratio, and triglyceride (TG) levels) of 142 subjects with probable or possible AD (mean age 76.5 ± 8.9 years), not on lipid lowering therapy by Apo E genotype. Assessment was done by gene status and gene dose. Results: ApoE4 gene status did not reveal any significant differences in the lipid profile except for LDL. However, significant differences were observed by ApoE gene dose. Conclusion: ApoE gene status has minimal influence on the lipid panel or mean age in AD. Apo E gene dose does influence the lipid panel with Apo E 2/2, and 2/3 having significantly better lipid panels and older age of onset. ©2006 Bentham Science Publishers Ltd

Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes

Brain deposits of amyloid β peptide (Aβ) have been a diagnostic hallmark of Alzheimer\u27s disease (AD) for nearly a century. Recent studies have demonstrated that Aβ is also present in peripheral blood. Here, we present evidence that circulating Aβ42 is subject to complement C3b-dependent adherence to complement receptor 1 (CR1) on erythrocytes, a classical set of mechanisms by which pathogens and proteins recognized as foreign are cleared from the bloodstream. Levels of Aβ42 targeted by this pathway differ significantly in AD compared to mild cognitive impairment and nondemented elderly controls. © 2005 Elsevier Inc. All rights reserved