Affiliations:
Institute of Basic and Translational Medicine & Shaanxi Key Laboratory of Brain Disorders, Xi’an Medical University, Xi’an, PR China
Correspondence:
[*]
Correspondence to: Xingchun Gou and Yuelin Zhang, Shaanxi Key Laboratory of Brain Disorders & Institute of Basic and Translational Medicine, Xi’an Medical University, No.1 Xinwang Road, Xi’an 710021, China. Tel.: +86 29 86177603; Fax: +86 29 86177603; E-mail: gouxingchun@189.cn. (X. Gou) and Zhangyuelin68@163.com. (Y. Zhang)
Note: [1
] These authors contributed equally to this work.
Abstract: Alzheimer’s disease (AD) is a chronic neurodegenerative disease that has been recognized as one of the most intractable medical problems with heavy social and economic costs. Amyloid-β (Aβ) has been identified as a major factor that participates in AD progression through its neurotoxic effects. The major mechanism of Aβ-induced neurotoxicity is by interacting with membrane receptors and subsequent triggering of aberrant cellular signaling. Besides, Aβ transporters also plays an important role by affecting Aβ homeostasis. Thus, these Aβ receptors and transporters are potential targets for the development of AD therapies. Here, we summarize the reported therapeutic strategies targeting Aβ receptors and transporters to provide a molecular basis for future rational design of anti-AD agents.
