Tadanori Hamano, Norimichi Shirafuji, Chiemi Makino, Shu-Hui Yen, Nicholas M Kanaan, Asako Ueno, Jinya Suzuki, Masamichi Ikawa, Akiko Matsunaga, Osamu Yamamura, Masaru Kuriyama, Yasunari Nakamoto
Tau aggregation and amyloid β protein (Aβ) deposition are the main causes of Alzheimer's disease (AD). Peroxisome proliferator-activated receptor γ (PPARγ) activation modulates Aβ production. To test whether the PPARγ agonist pioglitazone (PIO) is also effective in preventing tau aggregation in AD, we used a cellular model in which wild-type tau protein (4R0N) is overexpressed (M1C cells) (Hamano et al., 2012) as well as primary neuronal cultures. PIO reduced both phosphorylated and total tau levels, and inactivated glycogen synthase kinase 3β, a major tau kinase, associated with activation of Akt...
September 23, 2016: Biochemical and Biophysical Research Communications