title: Trafficking regulation of proteins in Alzheimer's disease.
abstract: The β-amyloid (Aβ) peptide has been postulated to be a key determinant in the pathogenesis of Alzheimer's disease (AD). Aβ is produced through sequential cleavage of the β-amyloid precursor protein (APP) by β- and γ-secretases. APP and relevant secretases are transmembrane proteins and traffic through the secretory pathway in a highly regulated fashion. Perturbation of their intracellular trafficking may affect dynamic interactions among these proteins, thus altering Aβ generation and accelerating disease pathogenesis. Herein, we review recent progress elucidating the regulation of intracellular trafficking of these essential protein components in AD.
authors.forename: Shangtong
authors.initials: S
authors.lastname: Jiang
authors.forename: Yanfang
authors.initials: Y
authors.lastname: Li
authors.forename: Xian
authors.initials: X
authors.lastname: Zhang
authors.forename: Guojun
authors.initials: G
authors.lastname: Bu
authors.forename: Huaxi
authors.initials: H
authors.lastname: Xu
authors.affiliation: Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian 361102, China. yunzhang@xmu.edu.cn.
authors.forename: Yun-wu
authors.initials: YW
authors.lastname: Zhang
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism*; D006801:Humans; D021381:Protein Transport / Q000502:physiology*