@article {Niikura1902, author = {Takako Niikura and Yuichi Hashimoto and Takashi Okamoto and Yoichiro Abe and Takashi Yasukawa and Masaoki Kawasumi and Takako Hiraki and Yoshiko Kita and Kenzo Terashita and Keisuke Kouyama and Ikuo Nishimoto}, title = {Insulin-Like Growth Factor I (IGF-I) Protects Cells from Apoptosis by Alzheimer{\textquoteright}s V642I Mutant Amyloid Precursor Protein through IGF-I Receptor in an IGF-Binding Protein-Sensitive Manner}, volume = {21}, number = {6}, pages = {1902--1910}, year = {2001}, doi = {10.1523/JNEUROSCI.21-06-01902.2001}, publisher = {Society for Neuroscience}, abstract = {It has been found that insulin-like growth factor I (IGF-I) exerts cytoprotection against Aβ amyloid-induced neuronal cell death. Deposits of Aβ amyloid are one of the pathological hallmarks of Alzheimer{\textquoteright}s disease (AD). Here, we examined whether IGF-I exerts protective activity against cell death induced by a familial AD (FAD)-linked mutant of amyloid precursor protein (APP), and we found that IGF-I protected cells from toxicity of FAD-associated V642I mutant of APP in multiple cell systems. IGFBP-3 blocked this action of IGF-I, but not of des(1-3)IGF-I, which was as active as IGF-I in the presence of IGFBP-3. The data also demonstrated that the IGF-I receptor (IGF-IR) mediates the protective activity of IGF-I. The antagonizing function of the IGF-I/IGF-IR system against V642I-APP, which is further antagonized by IGFBP-3, provides a molecular clue to the understanding of AD pathophysiology and to the establishment of potential therapy for AD.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/21/6/1902}, eprint = {https://www.jneurosci.org/content/21/6/1902.full.pdf}, journal = {Journal of Neuroscience} }