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    National Tsing Hua University Institutional Repository > 生命科學院  > 系統神經科學研究所 > 博碩士論文 >  在果蠅神經中表現人類LRRK2發現會影響其壽命,ATP和氧化壓力


    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/83154


    Title: 在果蠅神經中表現人類LRRK2發現會影響其壽命,ATP和氧化壓力
    Authors: 蕭秉諺
    Hsiao, Ping-Yen
    Chang, Hui-Yun
    教師: 張慧雲
    Date: 2013
    Keywords: LRRK2蛋白
    三磷酸腺苷
    LRRK2
    ATP
    氧化壓力
    壽命
    Oxidative stress
    Life-span
    Abstract: 帕金森氏症是一種常見的神經退化性疾病,明顯的病徵有顫抖和運動功能障礙。這些病徵是因為病人大腦黑質多巴胺神經元凋亡引起。在帕金森氏症中LRRK2是其中一個重要的致病基因,LRRK2突變大多和家族遺傳有關。帕金森氏症病人表現突變LRRK2會造成a-synuclein 或tau蛋白的累積。大多數研究都把焦點集中在突變的LRRK2,但是正常LRRK2的功能尚未釐清。因此我們利用Gal4/UAS系統在果蠅神經表現人類LRRK2,研究LRRK2的正常功能。在我們的實驗中,發現LRRK2表現在果蠅的大腦或多巴胺神經細胞會降低果蠅死亡率。LRRK2表現在果蠅的眼睛,可以對抗死亡基因hid, reaper導致的細胞凋亡。除此之外,我们研究人類LRRK2對果蠅大腦中ATP量和氧化壓力之影響,這些研究資料顯示LRRK2表現可以透過某些機制提高神經細胞的ATP量和抗氧化壓力。我顯示LRRK2表現可以透過某些機制提高神經細胞的ATP量和抗氧化壓力。總而言之,雖然突變LRRK2所引起帕金森氏症機制是非常重要的,但是研究正常LRRK2的功能可增加我們瞭解突變的LRRK2如何致病,且對未來的治療是非常有幫助的。
    Parkinson’s disease is one of the common neuron degeneration diseases. The obvious symptom was shacking and movement dysfunction that is caused by degeneration dopamine neuron in substantia nigra. Leucine-rich repeat kinase 2 (LRRK2) is an important gene association with Parkinson’s disease. Mutation in LRRK2, the most common known cause of autosomal dominant PD, is also found in ‘sporadic’ cases. PD patient’s brain tissue with LRRK2 mutations has accumulation of a-synuclein and/or tau protein aggregates. Many previous studies focus on mutation LRRK2; however, normal LRRK2 function remains unclear. Therefore, we investigated the role of LRRK2 through GAL4/UAS system, in Drosophila. In our studies, we found LRRK2 expression in fly brains or DA neurons can decrease Drosophila mortality. Furthermore, we found that LRRK2 expression can partially rescue apoptotic cell death induced by Grim, or Hid. Finally, we showed that LRRK2 expression in neurons can increase ATP levels and oxidative stress. Taken together, our results suggest that LRRK2 function is critical for neuronal survival which might be useful to realize how LRRK2 mutation mediates Parkinson’s disease due to (LOF) loss of function, and may help for future therapeutic intervention.
    URI: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/83154
    Source: http://thesis.nthu.edu.tw/cgi-bin/gs/hugsweb.cgi?o=dnthucdr&i=sGH029980583.id
    Appears in Collections:[系統神經科學研究所] 博碩士論文

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