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Kang, Min Suk,Baek, Seung-Hoon,Chun, Yoon Sun,Moore, A. Zenobia,Landman, Natalie,Berman, Diego,Yang, Hyun Ok,Morishima-Kawashima, Maho,Osawa, Satoko,Funamoto, Satoru,Ihara, Yasuo,Di Paolo, Gilbert,Par American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.29
<P>Amyloid β-peptide (Aβ) pathology is an invariant feature of Alzheimer disease, preceding any detectable clinical symptoms by more than a decade. To this end, we seek to identify agents that can reduce Aβ levels in the brain via novel mechanisms. We found that (20<I>S</I>)-Rg3, a triterpene natural compound known as ginsenoside, reduced Aβ levels in cultured primary neurons and in the brains of a mouse model of Alzheimer disease. The (20<I>S</I>)-Rg3 treatment induced a decrease in the association of presenilin 1 (PS1) fragments with lipid rafts where catalytic components of the γ-secretase complex are enriched. The Aβ-lowering activity of (20<I>S</I>)-Rg3 directly correlated with increased activity of phosphatidylinositol 4-kinase IIα (PI4KIIα), a lipid kinase that mediates the rate-limiting step in phosphatidylinositol 4,5-bisphosphate synthesis. PI4KIIα overexpression recapitulated the effects of (20<I>S</I>)-Rg3, whereas reduced expression of PI4KIIα abolished the Aβ-reducing activity of (20<I>S</I>)-Rg3 in neurons. Our results substantiate an important role for PI4KIIα and phosphoinositide modulation in γ-secretase activity and Aβ biogenesis.</P>