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頁籤選單縮合
題 名 | Genetic Polymorphism of Monoamine Oxidase B and Susceptibility of Parkinson's Disease=B型單胺氧化酶基因的多形性與巴金森氏病易感性的關連 |
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作 者 | 黃文柱; 賴明亮; 蔡子同; 賴明德; | 書刊名 | 中華醫學雜誌 |
卷 期 | 60:3 1997.09[民86.09] |
頁 次 | 頁137-141 |
分類號 | 415.83 |
關鍵詞 | B型單胺氧化酶基因的多形性; 巴金森氏病; 聚合酶連鎖反應; 單股去氧核糖核酸構型多形性分析; Monoamine oxidase B genetics; Parkinson's disease; Polymerase chain reaction; Single-stranded conformational polymorphism; |
語 文 | 英文(English) |
中文摘要 | 背景:就巴金森氏病所欠缺的神經傳導物質,病態生理以及在靈長類和人類的實驗與觀察,B型單胺氧化�t與巴金森氏病的致病原因及病情的進展有密切的關連。我們假定基因可以決定酵素的活性, 因而作了B型單胺氧化�t的基因多形性分析,並藉此找出那一種對偶基因或基因型在巴金森氏病患者出現的機率比正常人高。 方法:研究對象包括65位巴金森氏病患者及108位正常人。病人的診斷標準是依據腦內移植委員會提出的準則。我們利用puregene kit從受試者白血球中抽取去氧核糖核酸( DNA)。利用聚合�t連鎖反應(PCR)來擴大B型單胺氧化�t的基因,再以核酸內切限制�tHae Ⅲ來篩檢PCR的產物,並找出適當的片斷作單股DNA構型多形性分析。 結果:在單股 DNA 構型多形性分析時,我們可以看到 DNA 片斷因移動性不同而分為兩條帶狀區,分別稱為對偶基因1及對偶基因2。我們的研究顯示B型單胺氧化�t的基因型或對偶基因1或2在病人與正常人間出現的頻率無統計學上的差異。 結論:B型單胺氧化�t基因的多形性也存在於臺灣的巴金森氏病患者及正常人。但我們並沒有在患者身上發現某一種對偶基因出現的頻率有意義的升高。 因為這個研究只分析B型單胺氧化�t基因的一部份;所以雖然沒有找到兩者之間的關連性,但也不能完全排除B型單胺氧化�t基因在巴金森氏病的病因可能扮演的角色。 |
英文摘要 | Background: Monoamine oxidase B (MAO-B) may play a role in the progression and cause of parkinson's diesease (PD), given consideration of the biochemistry and pathophysiology of the disease, and experiments on primates and humans. Assuming that the structural gene determines enzyme activity, an association study was undertaken to examine MAO-B genetic polymorphisms and look for the unique MAO-B gene allele which occurred at a higher frequency in PD patients. Methods: Sixty-five PD patients, diagnosed according to the criteria set by a Core Assessment Program for Intracerebral Transplantations Committee, and 108 healthy controls were enrolled in this study. Genomic DNA was extracted from peripheral leukocytes by using a puregene kit. Polymerase chain reaction (PCR) was used to amplify the MAO-B genome. The PCR products wer screened by restriction enzyme Hae Ⅲ digestion and analyzed by single-stranded conformational polymorphism (SSCP). Results: Two bands with different mobility shifts, defined as MAO-B allele 1 and allele 2, were observed in SSCP analysis. Neither genotypes nor allelic frequencies of MAO-B showed a significant difference between PD patients and controls in our study. Conclusions: Polymorphism of MAO-B genome was demonstrated in this study. It failed to show an association of a genetic marker with PD. However, this did not necessarily exclude the MAO-B locus from playing a role in causing PD because a polymorphism different from the one evaluated here may show some disease association. |
本系統中英文摘要資訊取自各篇刊載內容。