| 研究生: |
劉芊宥 Liu, Chien-Yu |
|---|---|
| 論文名稱: |
乙醛脫氫酶2基因多型性與巴金森氏病患者認知功能之關係 Association of Aldehyde Dehydrogenase 2 Gene Polymorphism and Cognitive Function in Parkinson's Disease |
| 指導教授: |
余睿羚
Yu, Rwei-Ling |
| 學位類別: |
碩士 Master |
| 系所名稱: |
醫學院 - 行為醫學研究所 Institute of Behavioral Medicine |
| 論文出版年: | 2017 |
| 畢業學年度: | 105 |
| 語文別: | 中文 |
| 論文頁數: | 84 |
| 中文關鍵詞: | 巴金森氏病 、認知功能 、乙醛脫氫酶基因多型性 、ALDH2 、多巴胺 |
| 外文關鍵詞: | Parkinson’s Disease, cognitive function, ALDH2 gene polymorphism, dopamine |
| 相關次數: | 點閱:179 下載:5 |
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目的:過去研究顯示多巴胺濃度對巴金森氏病(巴病)患者認知功能扮演重要角色,而乙醛脫氫酶2(Aldehyde dehydrogenase 2, ALDH2)與多項神經傳導物質代謝有關,本研究欲探究ALDH2基因多型性(GG vs. AG/AA)於巴病患者各認知範疇表現之影響。
方法:研究參與者為54位原發性巴病患者,依據基因型分為GG組27人、AG/AA組27人。參與者個別於藥效有效狀態受測包含注意力(簡易心智量表-注意力、魏氏智力測驗-記憶廣度分測驗「順序部分」)、執行功能(史楚普字色作業、魏氏智力測驗-記憶廣度分測驗「逆序部分」、尼爾森修訂版卡片分類測驗、色彩路徑描繪測驗、語意流暢度測驗)、記憶力(魏氏記憶力測驗-邏輯記憶與圖繪記憶)、視空間能力(簡易心智量表-五角形仿繪)、語言能力(簡易心智量表-語言)之神經心理測驗,並接受抽血完成血液樣本之採集。
結果:本研究發現ALDH2基因多型性對不同認知範疇之影響有異。在語言功能(簡易心智量表書寫造句)上,GG組表現顯著較AG/AA組佳〖(x〗^2=4.320,p=0.038);而在執行功能之工作記憶部件(記憶廣度逆序部分)、模組轉換能力(尼爾森修訂版卡片分類測驗「完成分類數」),AG/AA組表現較GG組佳(U=484.0,p=0.034; U=549.0,p=0.001)。
討論:ALDH2基因多型性對巴病患者之認知功能表現有影響,不同ALDH2基因型於不同認知範疇之影響有異。推論於執行功能範疇,ALDH2 AG/AA組較GG組因多巴胺代謝效率較慢,故保留較多的多巴胺,在與背外側前額葉多巴胺濃度有關之執行功能作業表現較佳;於語言範疇,ALDH2 AG/AA組在「書寫造句」表現較GG組差,不排除有其他更高階認知元素或細緻的動作表現涉入影響其作業表現;於記憶範疇,ALDH2 GG組與AG/AA組記憶功能無顯著差異,本研究中所選用之記憶功能作業未能確認ALDH2基因多型性與巴病患者記憶功能表現之關係,尚待未來研究檢視ALDH2代謝神經毒素於巴病認知功能演進過程中扮演之角色。
This study aims to explore the association of aldehyde dehydrogenase 2 (ALDH2) gene polymorphism and cognitive function in Parkinson's disease (PD). The Asian-specific single nucleotide polymorphism rs671 causes reduced enzyme activity. A total of 54 PD patients were recruited. Each participant was assessed with medical characteristics and their ALDH2 genotype. Several neuropsychological tests were applied to assess five different cognitive domains including attention, executive function, language, memory, and visuospatial function. We found that ‘Mini-Mental State Examination (MMSE) - write a sentence’ were significantly lower in patients with inactive ALDH2 〖(x〗^2=4.320,p=0.038). On the contrary, the working memory substrate and set-shifting substrate of the executive function were significantly lower in patients with active ALDH2 (U=484.0,p=0.034; U=549.0,p=0.001). Cumulatively, these results demonstrate that ALDH2 gene polymorphism modulates cognitive function in PD patients by showing the behavioral consequences of genetic variation vary within different cognitive domains.
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