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中文摘要
翻译
在过去的一年里,我们试图确定鞘氨醇激酶/S1 P受体轴是否在神经退行性变中起重要作用。 我们使用了一个完善的Sandhoff小鼠模型的神经退行性病变,其中包括神经元凋亡,炎症和胶质增生。 为了确定S1 P的产生在神经退行性过程中是否重要,我们在Sandhoff模型中删除了Sphk 1基因。 我们发现,与Sphk 1基因正常的对照Sandhoff小鼠相比,这些小鼠的寿命和临床状况有显着改善。 这些结果表明,Sphk 1的表达可能有助于神经退行性过程。 未来的实验将解决改善疾病进程的机制。
英文摘要
This past year we have attempted to determine if the sphingosine kinase/S1P receptor axis has a significant role during neurodegeneration. We used a well-established Sandhoff mouse model of neurodegeneration, which included neuronal apoptosis, inflammation and gliosis. In order to determine if S1P production was important during the neurodegenerative process we deleted the Sphk1 gene in the Sandhoff model. We found a significant improvement in life span and clinical condition of these mice compared with the control Sandhoff mice with a normal Sphk1 gene. These results indicate that Sphk1 expression may have contributed to the neurodegenerative course. Future experiments will address the mechanism of the improved course of the disease.
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会议论文
Sphingolipid Biology of Inflammation and Immunity
Mouse Models of Novel Sphingolipid Biology and Disease Mechanisms
Sphingolipid Biology of Neurodegeneration
Sphingolipid Biology and Regulation of Metabolism
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Journal of Integrative Plant Biology
  • 批准号:
    31024801
  • 项目类别:
    专项基金项目
  • 资助金额:
    24.0万元
  • 批准年份:
    2010
  • 负责人:
    贺萍
  • 依托单位: