18.97.14.80
18.97.14.80
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β-Amyrin Ameliorates Alzheimer’s Disease-Like Aberrant Synaptic Plasticity in the Mouse Hippocampus
( Hye Jin Park ) , ( Huiyoung Kwon ) , ( Ji Hye Lee ) , ( Eunbi Cho ) , ( Young Choon Lee ) , ( Minho Moon ) , ( Mira Jun ) , ( Dong Hyun Kim ) , ( Ji Wook Jung )
UCI I410-ECN-0102-2021-500-000636432
* This article is free of use.

Alzheimer’s disease (AD) is a progressive and most frequently diagnosed neurodegenerative disorder. However, there is still no drug preventing the progress of this disorder. β-Amyrin, an ingredient of the surface wax of tomato fruit and dandelion coffee, is previously reported to ameliorate memory impairment induced by cholinergic dysfunction. Therefore, we tested whether β-amyrin can prevent AD-like pathology. β-Amyrin blocked amyloid β (Aβ)-induced long-term potentiation (LTP) impairment in the hippocampal slices. Moreover, β-amyrin improved Aβ-induced suppression of phosphatidylinositol-3-kinase (PI3K)/Akt signaling. LY294002, a PI3K inhibitor, blocked the effect of β-amyrin on Aβ-induced LTP impairment. In in vivo experiments, we observed that β-amyrin ameliorated object recognition memory deficit in Aβ-injected AD mice model. Moreover, neurogenesis impairments induced by Aβ was improved by β-amyrin treatment. Taken together, β-amyrin might be a good candidate of treatment or supplement for AD patients.

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGMENTS
REFERENCES
[자료제공 : 네이버학술정보]
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