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Aβ Metabolism and the Role of APOE in Alzheimer's Disease
Yue Miao Yin1,3#, Jing Du2# and Zhao Wang1*1MOE Key Laboratory of Protein Sciences, School of Pharmaceutical Sciences, Tsinghua University, Beijing 100084, People’s Republic of China
2Institute of Biomechanics and Medical Engineering, Department of Engineering Mechanics, School of Aerospace, Tsinghua University, Beijing 100084, People’s Republic of China
3Department of Pharmaceutics, Medical College of Qinghai University, Xining 810001, Qinghai Province, People’s Republic of China
- *Corresponding Author:
- Zhao Wang
MOE Key Laboratory of Protein Sciences
School of Pharmaceutical Sciences
Tsinghua University, Beijing 100084
People’s Republic of China
Tel: +86 10 62772241
E-mail: zwang@tsinghua.edu.cn
Received date: November 02, 2016; Accepted date: November 14, 2016; Published date: November 21, 2016
Citation: Yin YM, Du J, Wang Z (2016) Aβ Metabolism and the Role of ApoE in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 6:285. doi:10.4172/2161-0460.1000285
Copyright: © 2016 Yin YM, 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
Disturbance of the production and clearance of Aβ in the brain is the main cause of memory and cognition decline and contributes strongly to the development of AD. In human, APOE gene has three isoforms, ε2, ε3 and ε4, with APOE ε4 as the most risk gene among them. In the development of AD pathophysiology, ApoE4 is positively associated with Aβ plague formation, but the mechanisms are not clear. In this review, we proposed a hypothesis that the effect of ApoE4 on Aβ possibly involves three processes: 1) ApoE4 can directly interact with Aβ and interferes Aβ clearance. 2) ApoE4 can compete with Aβ for the same receptor, that hinds the cellular uptake pathways of Aβ. 3) ApoE4 also modulates other Aβ degrading proteases like IDE to downregulate Aβ degradation, but the mechanisms needs to be further investigated. These findings suggest that the effect of ApoE in AD pathogenesis is complicated and modulation of ApoE is an attractive strategy for AD therapy.
