Identification of potential Chinese herbs for Alzheimer’s disease using primary culture and mouse models

碩士 === 國立臺灣師範大學 === 生命科學系 === 104 === Alzheimer’s disease (AD) is the most common neurodegenerative disease associated with progressive damage in hippocampal neurons and cognitive dysfunctions. It is estimated that over 35 million people worldwide suffered from the disease. Both the accumulation of...

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Bibliographic Details
Main Authors: Huang, Chimg-Yi, 黃景怡
Other Authors: Hsieh, Hsiu-Mei
Format: Others
Language:zh-TW
Published: 2016
Online Access:http://ndltd.ncl.edu.tw/handle/33529384128197436380
Description
Summary:碩士 === 國立臺灣師範大學 === 生命科學系 === 104 === Alzheimer’s disease (AD) is the most common neurodegenerative disease associated with progressive damage in hippocampal neurons and cognitive dysfunctions. It is estimated that over 35 million people worldwide suffered from the disease. Both the accumulation of beta-amyloid peptides (Aβ) and tau protein phosphorylation are regarded as crucial events in the initiation of AD. Recently, more evidences show that the multi-target characteristics of traditional Chinese Herb Medicine (CHM) may be advantageous over single-target drugs against the multifactorial nature of AD. These drugs have therefore attracted much attention in the research and treatment in AD. In the present study, we established mouse primary hippocampal neuronal culture treated with oligomeric Aβ25-35 and Aβ42 as the screening platform of CHM. From the in vitro screening results , we found that CHM NH037 can prevent the decrease of neuronal number, neuritic length, branch number, lipid oxidation, amyloid deposition , and NH037 increasing the level of inactived GSK3β under neurotoxicity of oligomeric Aβ. Furthermore, the administration of NH037 also reduced anxiety and the cognitive impairment in the C57BL/6J mice treated with bilateral intrahippocampal CA1 injection of oligomeric Aβ25-35. From pathological analysis, we further found that the pretreatment of NH037 decreased the levels of Aβ deposition, tau protein phosphorylation, neuroinflammation, and increased the levels of synapse-related protein expression, noradrenergic and serotonergic neurons against the toxicity of oligomer Aβ25-35. Therefore, using CHM NH037 is a potential therapeutic strategy to prevent the cognitive, noncognitive dysfunction, and related pathogenic characterizations of AD.