碩士 / 臺北醫學大學 / 醫學研究所 / 92 / Parkinson''s disease (PD) is a neurodegenerative motor disorder that is characterized by the loss of dopaminergic neurons from the substantia nigra. The pathological mechanism of Parkinson’s disease is categorized in aging, environmental factor, and genetic disorders. In genetic research, there were more than 10 genes mutations identified in this disease. The first pathogenetic gene identified is α-synuclein, but its phathological mechanism is unknown. In previous study, it’s demonstrated that all synuclein isoforms expressed massively in early embryologic development of the central nervous system. These results revealed that synuclein may be essential to neurogenesis. In our research, we cloned synuclein of human, rat, and zebrafish. Using constructs containing synuclein and green fluorescent protein (GFP) genes drived by the neural-specific promoter, HuC, over-expressed in zebrafish neural system. In our study, it’s demonstrated that the intensity of fluorescence in human α-synuclein containing the A30P Parkinson''s disease mutation injected embryos decreased along with the growing days obviously, however, the same phenomenon was not found in human α-synuclein wild type and human α-synuclein containing the A53T Parkinson''s disease mutation injected embryos. Furthermore, we found that the expression of human α-synuclein wild type occurred dense and discrete dots in neurite, but the pattern found at the incidence of 37 % and 58 % in α-synuclein mutant A30P and A53T respectively. These results provided us some new directions in researches about the possible pathogenesis of PD and the property change in α-synuclein Parkinson''s disease mutation in the future.
Identifer | oai:union.ndltd.org:TW/092TMC00534007 |
Date | January 2004 |
Creators | Ching-Fang Liu, 劉靜芳 |
Contributors | Chih-Ming Chou, 周志銘 老師 |
Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
Language | zh-TW |
Detected Language | English |
Type | 學位論文 ; thesis |
Format | 83 |
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