目的探讨12月龄APP/PS1转基因小鼠学习记忆能力下降与胼胝体脱髓鞘损伤之间的关系。方法12只12月龄APP/PS1转基因小鼠为AD组,12只同窝阴性小鼠为野生组。Morris水迷宫检测两组学习记忆能力;卢卡斯快蓝染色观察胼胝体神经纤维形态;免疫组化检测胼胝体髓鞘碱性蛋白(MBP)含量;硫黄素S染色观察淀粉样斑块在胼胝体的沉积情况。结果与野生组相比,AD组逃避潜伏期明显延长(Z>2.873, P<0.01),穿越平台次数显著减少(t=-7.339, P<0.001)。AD组胼胝体神经纤维髓鞘稀疏,排列紊乱,出现较多空洞;MBP含量较野生组显著降低(t=-4.481, P<0.001);胼胝体区出现淀粉样斑块沉积。结论12月龄APP/PS1转基因小鼠学习记忆能力下降,可能与淀粉样斑块在胼胝体的沉积引起胼胝体神经纤维脱髓鞘损伤有关。
ObjectiveTo investigate the relationship between learning and memory deficit and demyelination of the corpus callosum in twelve-month old APP/PS1 transgenic mice. MethodsTwelve twelve-month old APP/PS1 transgenic mice were as AD group, and age-matched wild type (WT) littermates were as WT group. Learning and memory ability was tested with Morris water maze, and the morphology of nerve fiber of corpus callosum was detected with Luxol Fast Blue staining. Immunohistochemistry was used to detect myelin basic protein (MBP) in the corpus callosum. Thioflavine S staining was used to detect amyloid plaque in the corpus callosum. ResultsCompared with WT group, the latency increased (Z>2.873, P<0.01) and the times crossing the location of the platform decreased (t=-7.339, P<0.001) in AD group. The nerve fibers were sparse and disorganized, with a lot of vacuoles in the corpus callosum of AD group. The positive expression of MBP in the corpus callosum was significantly decreased (t=-4.481, P<0.001) in AD group compared with WT group. There were amyloid plaques in the corpus callosum of AD group. ConclusionTwelve-month old APP/PS1 transgenic mice exhibit learning and memory deficit, which may be attributed to the deposition of the amyloid plaque mediated demyelinated injury of the corpus callosum.
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