In vivo diffusion tensor imaging of amyloid-β-induced white matter damage in mice.
In vivo diffusion tensor imaging of amyloid-β-induced white matter damage in mice.
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DOI：
10.3233/jad-130236
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Shi WX
中科院分区：
文献类型：
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作者：
Sun SW;Liang HF;Mei J;Xu D;Shi WX
扩散张量成像（DTI）提示阿尔茨海默病（AD）前驱期存在白色物质异常。利用AD小鼠模型，通过活体DTI检测白色物质异常是否与功能缺陷和轴突损伤相关。将淀粉样蛋白β1-42（Aβ1-42）注入小鼠左侧脑室。注射后2个月，进行在体DTI和视觉诱发电位（VEP）记录，然后进行磷酸化神经丝和髓鞘碱性蛋白的免疫组化。Aβ1-42处理小鼠的DTI显示白色物质（包括视神经和视束）的径向扩散率显著增加。异常表现为VEP波幅降低、潜伏期延长。免疫组织化学证实了轴突和髓鞘完整性的显着损失。DTI可无创性检测Aβ1-42对小鼠白色物质的损伤。
Diffusion tensor imaging (DTI) suggests the presence of white matter abnormality at the prodromal stage in human Alzheimer’s disease (AD). To use a mouse model of AD to determine whether the white matter abnormality detected by in vivo DTI is associated with functional deficits and axon damage. Amyloid-β1–42 (Aβ1–42) was injected into the left lateral ventricle in mice. Two months after the injection, in vivo DTI and visual evoked potential (VEP) recordings were performed, followed by immunohistochemistry of phosphorylated neurofilament and myelin basic protein. DTI of Aβ1–42-treated mice showed a significant increase of radial diffusivity in white matter including the optic nerves and tracts. The abnormality was associated with decreased amplitude and increased latency of VEP. Immunohistochemistry confirmed a significant loss of axons and myelin integrity. White matter damage induced by Aβ1–42 in mice can be detected non-invasively by DTI.