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β-Asarone Mitigates Amyloidosis and Downregulates RAGE in a Transgenic Mouse Model of Alzheimer’s Disease

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Abstract

Elevated β-amyloid (Aβ) is a hallmark of Alzheimer’s disease (AD). Recent evidence has suggested that the receptor of advanced glycation end products (RAGE) is a key target for Aβ-induced perturbation in AD, and blockade of RAGE significantly alleviates synaptic injury. Our previous study has suggested that β-asarone could reduce neuronal apoptosis and improve memory deficits in β-amyloid precursor protein and presenilin-1 (APP/PS1) double transgenic AD-model mice. In the present study, we evaluated the effects of β-asarone on amyloidosis in APP/PS1 mice. We found that the survival of neurons of APP/PS1 mice was improved by β-asarone, meanwhile, β-asarone decreased Aβ deposition and down-regulated Aβ1–42 levels in cortex and hippocampus of APP/PS1 mice brain. Interestingly, the level of RAGE was also significantly down-regulated by β-asarone. Our findings suggest that β-asarone might be effective for the treatment of AD, and the decreasing effects of β-asarone on Aβ might associate with its down-regulation of RAGE.

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Acknowledgments

This work was supported by the National Major Science and Technology for Special Program of Creative Drug of China (2009ZX09103-429), the Doctoral Fund of Education Ministry of China (Nos. 20114425110007, 20134425110003), the Scientific and Technical innovation Project of Guangdong Provincial Education Department of China (2012KJCX0032), South China Chinese Medicine Collaborative Innovation Center (No. A1-AFD01514A05), and the Characteristic Key Discipline Construction Fund of Chinese Internal Medicine of Guangzhou University of Chinese Medicine (2013–2015).

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The authors declare that there is no conflict of interest.

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Correspondence to Shaoxiang Xian or Qi Wang.

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Cong Yang, Xiaoguang Li have contributed equally to this work.

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Yang, C., Li, X., Mo, Y. et al. β-Asarone Mitigates Amyloidosis and Downregulates RAGE in a Transgenic Mouse Model of Alzheimer’s Disease. Cell Mol Neurobiol 36, 121–130 (2016). https://doi.org/10.1007/s10571-015-0226-2

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