Wnt可通过mTOR调控mRNA翻译，促进细胞生长，其信号通路中的多个基因已被发现是儿童自闭症的易感基因。脆性X相关震颤/共济失调综合征(FXTAS)是因FMR1基因前突变所致的神经变性疾病，严重时可表现出自闭症状，异常增多的FMR1 mRNA是其发病的重要因素。最近的研究发现mTOR底物s6k1的过表达对FXTAS具有神经保护作用。在本课题中，我们拟利用免疫荧光、RNA干扰、免疫印迹等方法，研究Wnt过表达对FXTAS转基因果蝇是否具有神经保护作用，明确其作用是否与通过激活mTOR促进了FMR1 mRNA的有效翻译有关；并进一步研究Wnt过表达是否同时促进了FXTAS转基因果蝇自闭症状的发生，明确自闭症状的发生是否是FXTAS疾病保护性激活mTOR信号通路后的副产品，为寻找有效治疗FXTAS运动症状又避免诱发自闭症状的平衡提供理论依据。

Wnt can regulate mRNA translation through mTOR to promote cell growth, and its signaling pathway in multiple genes have been found to be susceptible genes of children with autism. Fragile X-associated tremor / ataxia syndrome (FXTAS) ，a neurodegenerative diseases, is caused by the FMR1 gene mutation , which can show autism,the abnormal increase in FMR1 mRNA is an important factor in its pathogenesis. Recently, studies have found that mTOR substrates s6k1 overexpression have neuroprotective effects for FXTAS. In the present study, we will definite whether Wnt overexpression have neuroprotective effects of FXTAS transgenic drosophila through many different methods including immunofluorescence, RNA interference and immunoblotting methods, then determinate whether there are close relationships between its role and activation of mTOR promoting the effective translation of FMR1 mRNA ;and further research whether Wnt overexpression promote the autism occurrence of FXTAS transgenic drosophila ,and confirm whether the occurrence of autism is the byproduct of FXTAS protection activating mTOR signaling pathway. Present study will offer a new theoretical basis for the balance between searching an effective treatment of FXTAS motor symptoms and avoid inducing autism.