Alzheimer's disease (AD) is a progressive and complex neurodegenerative disease in which the γ-secretase- mediated amyloid-β (Aβ) pathology plays an important role. We found that a multifunctional protein, β-...
Supplementary information is linked to the online version of the paper on the Cell Research website.Acknowledgments We thank Dr David Westaway (University of Alberta) for TgCRND8 mice, Dr David Baltimore (California Institute of Technology) for lentiviral constructs, Dr Raphael Kopan (Washington University) for the plasmid of myc-tagged NotchAE and Dr Johan Lundkvist (Karolinska Institutet) for the plasmid of Gal4-driven luciferase reporter gene, the plasmid of APP/CTFI3-GVP and NAE-GVP. We appreciate Shunmei Xin, Shan Chen and Xianglu Zeng for their technical assistance. We thank all members of the lab for sharing reagents and advice. This research was supported by the Ministry of Science and Technology (2009ZX09103-684), the National Natural Science Foundation of China (30621091, 30625014, 30623003, 30871285 and 90713047), the Shanghai Municipal Commission for Science and Technology (07PJ14099 and 09JC1416400), and the Chinese Academy of Sciences (2007KIP204).
Dysregulation of β-site APP-cleaving enzyme (BACE) and/or γ-secretase leads to anomalous production of amyloid-β peptide (Aβ) and contributes to the etiology of Alzheimer's disease (AD). Since these secreta...