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Article Publish Status: FREE
Abstract Title:

Oridonin Attenuates Synaptic Loss and Cognitive Deficits in an Aβ1-42-Induced Mouse Model of Alzheimer's Disease.

Abstract Source:

PLoS One. 2016 ;11(3):e0151397. Epub 2016 Mar 14. PMID: 26974541

Abstract Author(s):

Sulei Wang, Linjie Yu, Hui Yang, Chaosheng Li, Zhen Hui, Yun Xu, Xiaolei Zhu

Article Affiliation:

Sulei Wang

Abstract:

Synaptic loss induced by beta-amyloid (Aβ) plays a critical role in the pathophysiology of Alzheimer's disease (AD), but the mechanisms underlying this process remain unknown. In this study, we found that oridonin (Ori) rescued synaptic loss induced by Aβ1-42 in vivo and in vitro and attenuated the alterations in dendritic structure andspine density observed in the hippocampus of AD mice. In addition, Ori increased the expression of PSD-95 and synaptophysin and promoted mitochondrial activity in the synaptosomes of AD mice. Ori also activated the BDNF/TrkB/CREB signaling pathway in the hippocampus of AD mice. Furthermore, in theMorris water maze test, Ori reduced latency and searching distance and increased the number of platform crosses in AD mice. These data suggest that Ori might prevent synaptic loss and improve behavioral symptoms in Aβ1-42-induced AD mice.

Study Type : Animal Study

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