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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/S1P受体轴在神经退行性变过程中是否起着重要作用。我们使用了一种成熟的桑德霍夫小鼠神经变性模型,包括神经元凋亡、炎症和胶质细胞增生。为了确定S1P的产生是否在神经退行性变过程中起重要作用,我们在Sandhoff模型中删除了Sphk1基因。我们发现,与携带正常Sphk1基因的桑德霍夫小鼠相比,这些小鼠的寿命和临床状况都有显著改善。这些结果表明,Sphk1的表达可能参与了神经退行性变的过程。未来的实验将解决改善病程的机制。
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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Sphingolipid Biology of Neurodegeneration
Mouse Models of Novel Sphingolipid Biology and Disease Mechanisms
Sphingolipid Biology of Inflammation and Immunity
Mouse Models of Novel Sphingolipid Biology and Disease Mechanisms
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海外基金
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: