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系統識別號 U0026-2907201922295000
論文名稱(中文) 探索腦衰反應調節蛋白5(CRMP5) 對阿茲海默氏症小鼠社交缺失和記憶損傷的影響
論文名稱(英文) Exploring the effects of collapsin response mediator protein 5 (CRMP5) on social deficits and memory impairment in a mouse model of Alzheimer's disease
校院名稱 成功大學
系所名稱(中) 藥理學研究所
系所名稱(英) Department of Pharmacology
學年度 107
學期 2
出版年 108
研究生(中文) 林永舜
研究生(英文) Yung-Shuen Lin
學號 S26061096
學位類別 碩士
語文別 英文
論文頁數 59頁
口試委員 指導教授-蕭雅心
口試委員-簡伯武
口試委員-陳柏熹
中文關鍵字 阿茲海默氏症  社交缺失  海馬迴  CRMP5  GluA2 subunits  內吞作用 
英文關鍵字 Alzheimer’s disease  Social impairment  Hippocampus  CRMP5  GluA2 subunits  Endocytosis 
學科別分類
中文摘要 阿茲海默氏症乃神經退行性疾病中最為常見的一種病症之一,其有數種行為障礙,最廣為人知的特徵即為認知功能下降。除此之外,阿茲海默氏症亦有多種心理病徵,如譫妄、情緒失調以及冷漠。其中冷漠常表現出缺乏動機、喪失興趣以及社交問題等多種特徵。而過往相關研究指出,缺乏社交互動會造成阿茲海默氏症病患的病程加速;然而,擁有良好社交互動者其記憶障礙損壞的情況較為延緩。據以上現象推估,社交障礙也許是了解阿茲海默氏症病因之關鍵。腦衰反應調節蛋白5 (CRMP5)是腦衰反應調節蛋白家族的一員,其大量表現於腦中並與神經退行性疾病和心理疾病息息相關。曾有研究指出其與壓力誘導的社交行為缺失以及精神病徵有所關聯,亦被報導其在海馬迴這個掌管記憶能力與情緒表達的腦區中,於神經突及樹突生長上扮演要角。然而其在阿茲海默氏症上有何功能卻尚未被查明。因此,本篇研究意旨於探討CRMP5在阿茲海默氏症小鼠模型的社交行為及記憶功能缺失上究竟扮演何種角色。在過程中,我們首先發現了九個月大的3xTg-AD小鼠與控制組的B6129S小鼠相比表現出了顯著性的社交缺失,且在其海馬迴中,CRMP5表現量亦出現顯著上升。而當CRMP5表現量下降時,3xTg-AD小鼠的社交缺失現象獲得緩解;在CRMP5表現量上升時,3xTg-AD及B6129S小鼠皆有顯現社交缺失行為。有趣的是,在減少CRMP5表現量後,3xTg-AD小鼠的記憶能力有明顯回升;且CRMP5表現量上升時,僅有3xTg-AD小鼠記憶功能出現顯著性障礙。再者,我們確認了CRMP5會調控突觸上GluA2 subunits的表面表現量。以上所有發現證明了CRMP5可藉由調整突觸表面的GluA2表現來調控3xTg-AD小鼠的社交行為,並影響其記憶功能。
英文摘要 Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterized by several behavioral disturbances, especially cognitive decline. In addition to cognitive decline, AD also exhibits several psychiatric symptoms such as delusion, emotional changes, and apathy. Remarkably, apathy in AD is characterized by lacking motivation, loss of interesting, and social problems. It is worth noting that decreased social activity would accelerate AD progression, whereas enhanced social interactions could rescue AD-induced memory impairment. Thus, social impairment may be a key factor in explaining the etiology of AD. Collapsin response mediator protein 5 (CRMP5), one of the CRMP members, expresses abundantly in the brain and is involved in the mental disorders and neurodegenerative diseases. Previous studies suggest that CRMP5 is involved in neurite outgrowth and dendrite development in the hippocampus, which is a pivotal brain area for regulating memory, emotional and behavioral presentation. However, the specific functions of CRMP5 in AD are still unclear. Thus, this study aimed to explore the roles of CRMP5 in the social behaviors and memory performances of the 3xTg-AD mouse model. Here, we showed that 9-month-old 3xTg-AD mice exhibited social behavioral deficits and higher hippocampal CRMP5 levels than control (B6129S) mice. Knockdown of CRMP5 reversed the social deficits in 9-month-old 3xTg-AD mice, whereas CRMP5 overexpression decreased social interaction in both 3xTg-AD and control mice at 6 months of age. Interestingly, decreased CRMP5 rescued AD-induced memory impairment, but overexpression of CRMP5 accelerated memory loss only in 3xTg-AD mice. Moreover, we also found that surface GluA2 levels were affected by manipulations of CRMP5 expressions. These results demonstrated that CRMP5 expressions could regulate the social behaviors via modulation of the surface GluA2 trafficking and affected the memory performances in 3xTg-AD mice.
論文目次 中文摘要 …………………………………………………………………I
英文摘要 …………………………………………………………………III
致謝…………………………………………………………………………VI
縮寫索引表 ………………………………………………………………2
圖表索引 …………………………………………………………………4
Chapter 1 Introduction …………………………………………………6
Chapter 2 Specific aims …………………………………………………15
Chapter 3 Materials and Methods ……………………………………17
Chapter 4 Results …………………………………………………24
Chapter 5 Discussion …………………………………………………46
References ………………………………………………………………50
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