Liang Shengxiang, Huang Jia, Liu Weilin, Jin Hao, Li Long, Zhang Xiufeng, Nie Binbin, Lin Ruhui, Tao Jing, Zhao Shujun, Shan Baoci, Chen Lidian
College of Physical Science and Technology, Zhengzhou University, Zhengzhou 450001, China; College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China; Division of Nuclear Technology and Applications, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China; Beijing Engineering Research Center of Radiographic Techniques and Equipment, Beijing 100049, China.
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Behav Brain Res. 2017 Sep 29;335:26-31. doi: 10.1016/j.bbr.2017.08.005. Epub 2017 Aug 8.
Alzheimer's disease (AD) is characterized by neuropathological changes and progressive cognitive decline, which is associated with the volume loss and neurochemical alterations. However, the specific neurochemical alterations in cerebral regions that contribute to cognitive decline still remain unknown. In the present study, we measured cerebral morphological and neurochemical alterations using structural magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (H-MRS) in an AD model of APP/PS1 transgenic mice. Voxel-based morphometry (VBM) analysis indicated atrophy of the hippocampus, motor cortex, striatum, amygdaloid body, septal area, bed nucleus of the stria terminalis and accumbens nucleus in APP/PS1 transgenic mice. Furthermore, the hippocampus was selected as a region of interest (ROI) to explore neurochemical metabolism. The results showed that the ratios of N-acetylaspartate/creatine (NAA/Cr) and glutamate/creatine (Glu/Cr) were reduced, while myo-inositol/creatine (mIn/Cr) was increased in APP/PS1 transgenic mice compared to the wild type mice and accompanied by a decline in learning and memory. Taken together, the present study suggests that hippocampal atrophy and neurochemical changes in NAA, Glu and mIn may play a causative role in the cognitive decline associated with AD.
阿尔茨海默病（AD）的特征是神经病理变化和进行性认知衰退，这与脑容量减少和神经化学改变有关。然而，导致认知衰退的脑区中具体的神经化学改变仍不清楚。在本研究中，我们使用结构磁共振成像（MRI）和质子磁共振波谱（H-MRS）在APP/PS1转基因小鼠的AD模型中测量了脑形态和神经化学改变。基于体素的形态学测量（VBM）分析表明，APP/PS1转基因小鼠的海马体、运动皮层、纹状体、杏仁体、隔区、终纹床核和伏隔核萎缩。此外，选择海马体作为感兴趣区域（ROI）来探索神经化学代谢。结果显示，与野生型小鼠相比，APP/PS1转基因小鼠的N-乙酰天门冬氨酸/肌酸（NAA/Cr）和谷氨酸/肌酸（Glu/Cr）比值降低，而肌醇/肌酸（mIn/Cr）升高，并伴有学习和记忆能力下降。综上所述，本研究表明海马体萎缩以及NAA、Glu和mIn的神经化学变化可能在与AD相关的认知衰退中起因果作用。
