Beta Amyloid Peptide: Beta Amyloid Peptide: Research Paper: β-Asarone improves learning and memory in Aβ 1-42-induced Alzheimer's disease rats by regulating PINK1-Parkin-mediated mitophagy

Beta Amyloid Peptide: Research Paper: β-Asarone improves learning and memory in Aβ 1-42-induced Alzheimer's disease rats by regulating PINK1-Parkin-mediated mitophagy

β-Asarone improves learning and memory in Aβ 1-42-induced Alzheimer's disease rats by regulating PINK1-Parkin-mediated mitophagy

Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disease that is characterized by the extracellular accumulation of β-amyloid (Aβ). Many studies have shown a close relationship between autophagy and the formation of Aβ. As AD develops and progresses, mitophagy diminishes insoluble Aβ, and mitochondrial dysfunction seems to be a determining factor in the pathogenesis of AD. In our previous study, we showed that β-asarone pharmacological effects in APP/PS1 transgenic mice, reducing Aβ expression. However, the specific mechanism of this effect remains unclear. In this study, AD model rats induced by intracerebroventricular injection of Aβ1-42 were randomly divided into nine groups, and medical intervention was applied to the animals for 30 days. Subsequently, spatial learning and memory were evaluated by the water maze test. Bcl-2 levels in the hippocampus were determined by western blotting (WB). The protein expression of Aβ1-42, Beclin-1, p62, PINK1, and Parkin was assessed by WB and immunohistochemistry (IHC). The data showed that after β-asarone treatment, the learning and memory of the AD rats were clearly improved compared with those of the model group. Moreover, β-asarone decreased Aβ1-42, Bcl-2, and p62 levels but increased Beclin-1 levels compared with those in the model group. In addition, we treated a group of rats with CsA to inhibit mitophagy. β-Asarone increased PINK1 and Parkin expression compared with that in the model group. The results showed that β-asarone can improve the learning and memory of rats with Aβ1-42-induced AD by effectively promoting PINK1-Parkin-mediated mitophagy. Taken together, these results suggest that β-asarone may have the capacity to become a pharmaceutical agent for the treatment of AD in the future.

Keywords: Alzheimer's disease; Mitophagy; PINK1/Parkin; β-Asarone.


This article originally appeared in the "https://pubmed.ncbi.nlm.nih.gov/32556928/" and has their copyrights. We do not claim copyright on the content. This information is for research purposes only. This Blog is made available by publishers for educational purposes only as well as to give you general information and a general understanding , not to provide specific advice. By using this blog site you understand that there is no client relationship between you and the Blog publisher. The Blog should not be used as a substitute for competent research advice.  




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