Chao Feng-Lei, Zhang Lei, Zhang Yi, Zhou Chun-Ni, Jiang Lin, Xiao Qian, Luo Yan-Min, Lv Fu-Lin, He Qi, Tang Yong
Department of Histology and Embryology, Chongqing Medical University, Chongqing 400016, PR China; Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing 400016, PR China.
Department of Histology and Embryology, Chongqing Medical University, Chongqing 400016, PR China; Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing 400016, PR China.
Brain Res. 2018 Apr 1;1684:50-59. doi: 10.1016/j.brainres.2018.01.007. Epub 2018 Jan 6.
Neurogenesis might influence oligodendrogenesis and selectively instruct myelination in the mammalian brain. Running exercise could induce neurogenesis and protect the myelin sheaths in the dentate gyrus of AD mice. It is unclear whether running exercise can protect myelin sheaths in the absence of neurogenesis in the hippocampus of AD mice. Six-month-old male APP/PS1 transgenic mice were randomly assigned to a control group (Tg control) or a running group (Tg runner), and age-matched non-transgenic littermates were used as a wild-type group (WT control). The Tg runner mice were subjected to a running protocol for four months. The behaviors of the mice in the three groups were then assessed using the Morris water maze, and related quantitative parameters of the myelin sheaths within the CA1 field were investigated using unbiased stereological and electron microscopy techniques. Learning and spatial memory performance, CA1 volume, the volumes of the myelinated fibers, and myelin sheaths in the CA1 field were all significantly worse in the Tg control mice than in the WT control mice. Learning and spatial memory performance, CA1 volume and the volume of the myelin sheaths in the CA1 field were all significantly greater in the Tg runner mice than in the Tg control mice. These results reveal demyelinating lesions in the CA1 field of Alzheimer's disease (AD) mice and indicate that running exercise could protect against myelin sheath degeneration in the absence of neurogenesis, thereby reducing CA1 atrophy and delaying the onset and progression of AD.
神经发生可能会影响少突胶质细胞生成，并选择性地指导哺乳动物大脑中的髓鞘形成。跑步运动可以诱导神经发生，并保护AD小鼠齿状回中的髓鞘。目前尚不清楚在AD小鼠海马区缺乏神经发生的情况下，跑步运动是否能保护髓鞘。将6个月大的雄性APP/PS1转基因小鼠随机分为对照组（Tg对照）或跑步组（Tg跑步者），并将年龄匹配的非转基因同窝小鼠作为野生型组（WT对照）。对Tg跑步者小鼠进行为期四个月的跑步方案。然后使用莫里斯水迷宫评估三组小鼠的行为，并使用无偏立体学和电子显微镜技术研究CA1区域内髓鞘的相关定量参数。Tg对照小鼠的学习和空间记忆表现、CA1体积、髓鞘纤维体积以及CA1区域的髓鞘均明显比WT对照小鼠差。Tg跑步者小鼠的学习和空间记忆表现、CA1体积以及CA1区域的髓鞘体积均明显大于Tg对照小鼠。这些结果揭示了阿尔茨海默病（AD）小鼠CA1区域的脱髓鞘病变，并表明在缺乏神经发生的情况下，跑步运动可以防止髓鞘变性，从而减少CA1萎缩并延缓AD的发病和进展。
