Trafficking regulation of proteins in Alzheimer's disease

Shangtong Jiang, Yanfang Li, Xian Zhang, Guojun Bu, Huaxi Xu, Yun Wu Zhang*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

127 Citations (Scopus)

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.

Original languageEnglish
Article number6
JournalMolecular Neurodegeneration
Volume9
Issue number1
DOIs
Publication statusPublished - 11 Jan 2014
Externally publishedYes

Keywords

  • A Disintegrin and Metalloprotease 10
  • Alzheimer's disease
  • Amyloid beta (A4) precursor protein
  • Beta-site APP-cleaving enzyme 1
  • Trafficking
  • α-secretase
  • β-secretase
  • γ-secretase

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