Affiliations: [a] Shaanxi Key Laboratory of Brain Disorders and School of Basic Medical Science, Xi’an Medical University, Xi’an, China
| [b] Institute of Basic and Translational Medicine, Xi’an Medical University, Xi’an, China
Correspondence:
[*]
Correspondence to: Xingchun Gou and Fan Cheng, Shaanxi Key Laboratory of Brain Disorders and School of Basic Medical Science, Xi’an Medical University, No. 1 Xinwang Road, Xi’an 710021, China. Tel.: +86 29 86177603; Fax: +86 29 86177603; [email protected] (X. Gou); [email protected] (F. Cheng).
Note: [1] These authors contributed equally to this work.
Abstract: Aging societies have high incidence rates of Alzheimer’s disease (AD). AD is diagnosed at later disease stages and has a poor prognosis, and effective drugs and treatments for AD are lacking. The molecular mechanism of AD is not clear, and current research focuses primarily on amyloid-β (Aβ) deposition and tau protein hyperphosphorylation. Aβ deposition is the most frequently hypothesized initiating factor of AD, and Aβ clearance during the pathogenesis of AD may be an optional strategy to suppress AD development. Monocytes play important roles in the peripheral clearance of Aβ. Therefore, the present review summarizes our current knowledge of the potential roles of infiltrating macrophages, circulating monocytes, and Kupffer cells in the peripheral clearance of Aβ in AD.
