由異常的聚麩醯胺擴增所造成的神經退化性病變中，亨丁頓氏舞蹈症為具有高外顯性、發生率高的主要疾病之一。亨丁頓氏舞蹈症是由人類第四對染色體的IT15基因上，其第1號外引子發生不正常的CAG三核苷酸擴增導致。在細胞分子的層次上，亨丁頓氏舞蹈症的致病機轉雖尚未完全釐清，但是近年來在細胞、大鼠疾病模式以及病患檢體中都新發現了蛋白質磷酸酶B（PKB/Akt）可以磷酸化具有異常聚麩醯胺擴增的亨丁頓蛋白，進而減低其對於神經細胞的傷害與毒性。蛋白質磷酸酶B在神經細胞中可以藉由磷酸化其下游受質，包括參與細胞死亡機制的BAD，mTOR等蛋白因子，進而達成促使細胞生長、抑制細胞自戕的目的。加以其上游被蛋白質去磷酸酶2A（PP2A）藉由磷酸化與否來調控其活化態的呈現多寡與否。本實驗設計主要是利用在不同遺傳背景下的亨丁頓氏舞蹈症果蠅模式株，來探討蛋白質磷酸酶B、蛋白質去磷酸酶2A（包括B及C次單元）對於具有異常聚麩醯胺擴增的亨丁頓蛋白所造成的病理性狀有何影響。進而利用分子檢測技術判斷細胞分子層次上的各項變化（蛋白質表現量、蛋白質的活化態等），以期釐清亨丁頓氏舞蹈症，甚而推廣至聚麩醯胺疾病的致病機轉和可能的治療方向。

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