Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.
Neurobiol Aging. 2011 Dec;32(12):2324.e1-6. doi: 10.1016/j.neurobiolaging.2010.08.014. Epub 2010 Oct 22.
APPPS1 transgenic mice develop amyloid-β 42 (Aβ42)-driven early-onset cerebral β-amyloidosis. Stereological analysis of neocortical neuron number in groups of 2-, 10-, and 17-month-old APPPS1 mice did not reveal any changes compared with wild-type control animals despite massive amyloid-β (Aβ) load and disrupted cytoarchitecture. However, in subregions with high neuron density such as the granule cell layer of the dentate gyrus, modest but significant neuron loss was found, reminiscent of findings in previously published mouse models with late onset cerebral β-amyloidosis and predominant amyloid-β 40 (Aβ40) expression.
APPPS1 转基因小鼠出现淀粉样蛋白β42（Aβ42）驱动的早发性脑β-淀粉样变性。对 2 月龄、10 月龄和 17 月龄 APPPS1 小鼠与野生型对照动物的新皮质神经元数量进行的立体学分析显示，尽管淀粉样蛋白（Aβ）负荷量很大且细胞结构紊乱，但与野生型对照动物相比，并无明显变化。然而，在神经元密度较高的脑区，如齿状回颗粒细胞层，发现了适度但显著的神经元丢失，这与以前发表的具有晚发性脑β-淀粉样变性和以淀粉样蛋白β40（Aβ40）表达为主的小鼠模型的发现相似。
