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Role of LDL Cholesterol and Endolysosomes in Amyloidogenesis and Alzheimerís Disease | OMICS International | Abstract
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
Open Access

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Review Article

Role of LDL Cholesterol and Endolysosomes in Amyloidogenesis and Alzheimer’s Disease

Xuesong Chen*, Liang Hui, and Jonathan D Geiger

Department of Basic Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203, USA

Corresponding Author:
Xuesong Chen
Department of Basic Biomedical Sciences
University of North Dakota
School of Medicine and Health Sciences
504 Hamline St Grand Forks
North Dakota 58203 USA
Tel: (701) 777-0919
Fax: (701) 777-0387
E-mail: [email protected]

Received date: July 14, 2014; Accepted dat: September 16, 2014; Published date: September 22, 2014

Citation: Chen X, Hui L, Geiger J (2014) Role of LDL Cholesterol and Endolysosomes in Amyloidogenesis and Alzheimer’s Disease. J Neurol Neurophysiol 5:236. doi:10.4172/2155-9562.1000236

Copyright: © 2014 Chen X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The pathogenesis of late-onset sporadic Alzheimer’s disease (AD) is believed to result from complex interactions
between nutritional, environmental, epigenetic and genetic factors. Among those factors, altered circulating
cholesterol homeostasis, independent of the APOE genotype, continues to be implicated in brain deposition of
amyloid beta protein (Aβ) and the pathogenesis of AD. It is believed that trafficking of amyloid beta precursor protein
(AβPP) into endolysosomes appears to play a critical role in determining amyloidogenic processing of AβPP
because this is precisely where two enzymes critically important in AβPP metabolism are located; beta amyloid
converting enzyme (BACE-1) and gamma secretase enzyme. We have shown that elevated levels of LDL
cholesterol promote AβPP internalization, disturb neuronal endolysosome structure and function, and increase Aβ
accumulation in neuronal endolysosomes. Here, we will further discuss the linkage between elevated levels of LDL
cholesterol and AD pathogenesis, and explore the underlying mechanisms whereby elevated levels of plasma LDL
cholesterol promote amyloidogenesis.

Keywords

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