Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 47, Issue 12, Pages 1018-1022Publisher
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gmv106
Keywords
Alzheimer's disease; geniposide; GSK-3 beta; leptin; tau
Categories
Funding
- National Natural Science Foundation of China [81173063]
- Chongqing Science Found for Distinguished Young Scholars from Chongqing Science & Technology Community [2014jcyjjq10003]
- Innovation of Science and Technology Leading Talent in Chongqing from Chongqing Science & Technology Community [2014kjcxljrc0009]
- Chongqing Natural Science Foundation (Chongqing Science & Technology Community) [2013jjb10032]
- Innovative Research Team Development Program in University of Chongqing [KJTD 201314]
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We have previously demonstrated that geniposide attenuates the production of A beta(1-42) both in vitro and in vivo via enhancing leptin receptor signaling. But the role played by geniposide in the phosphorylation of tau and its underlying molecular mechanisms remain unclear. In this study, we investigated the effect of geniposide on the phosphorylation of tau and the role of leptin signaling in this process. Our data suggested that, accompanied by the up-regulation of leptin receptor expression, geniposide significantly decreased the phosphorylation of tau in rat primary cultured cortical neurons and in APP/PS1 transgenic mice, and this geniposide-induced decrease of tau phosphorylation could be prevented by leptin antagonist (LA). Furthermore, LA also prevented the phosphorylation of Akt at Ser-473 site and GSK-3 beta at Ser-9 site induced by geniposide. All these results indicate that geniposide may regulate tau phosphorylation through leptin signaling, and geniposide may be a promising therapeutic compound for the treatment of Alzheimer's disease in the future.
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