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 language | English (US) |
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Article number | 6 |
Journal | Molecular neurodegeneration |
Volume | 9 |
Issue number | 1 |
DOIs | |
State | Published - Jan 11 2014 |
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
ASJC Scopus subject areas
- Molecular Biology
- Clinical Neurology
- Cellular and Molecular Neuroscience