7.0T高场强功能核磁评估阿尔茨海默病动物模型海马神经元的变化

SICENCE新闻发布作者：张磊稿号：N2013050117.0T高场强功能核磁评估阿尔茨海默病动物模型海马神经元的变化磁共振波谱成像是利用磁共振现象和化学位移作用，进行无创性无放射性活体组织监测，可反映组织内生化及代谢变化。高场强(≥7.0T)磁共振波普成像具有较高的图像空间分辨率和密度分辨率，可对活体进行显微成像，不仅扫描结果分辨率高，结果精度高，扫描时间也明显缩短。中国首都医科大学附属北京天坛医院张磊所在团队完成的一项研究应用7.0T高场强功能核磁观察发现，阿尔茨海默病模型大鼠海马区N-乙酰天冬氨酸波峰减低，肌酸及胆碱波峰升高，与海马区切片苏木精-伊红染色所见神经元丢失，胶质细胞及小胶质细胞明显增生，海马萎缩结果一致；透射电镜扫描结果也证实模型组大鼠海马神经元突触小泡体积变小，突触结构不完整及数量明显减少。因此作者认为应用7.0T高场强核磁共振对阿尔茨海默病模型大鼠脑部进行显微成像，能够成为无创性评估阿尔茨海默病动物模型的的新手段。相关结果发表于《中国神经再生研究（英文版）》杂志2014年2月第4期。阿尔茨海默病模型建立2周后大鼠MRIT2加权影像未出现明显变化Article:7.0Tnuclearmagneticresonanceevaluationoftheamyloidbeta(1–40)animalmodelofAlzheimer’sdisease:comparisonofcytologyverifcation,byLeiZhang1,ShuaiDong2,GuixiangZhao3,YuMa4(1MRNeuroradiologyRoom,BeijingTiantanHospitalAffliatedtoCapitalMedicalUniversity,Beijing,China;2DepartmentofNeurology,SixthPeople’sHospitalofJinan,Jinan,ShandongProvince,China;3DepartmentofRehabilitationMedicine,SixthPeople’sHospitalofJinan,Jinan,ShandongProvince,China;4TsinghuaUniversityYuquanHospital,Beijing,China)ZhangL,DongS,ZhaoGX,MaY.7.0Tnuclearmagneticresonanceevaluationoftheamyloidbeta(1–40)animalmodelofAlzheimer’sdisease:comparisonofcytologyverification.NeuralRegenRes.2014;9(4):430-435.欲获更多资讯：NeuralRegenResSICENCE新闻发布作者：张磊稿号：N2013050117.0TNMRassesseschangesinhippocampalneuronsinanimalmodelsofAlzheimer’sdiseaseMagneticresonancespectroscopycanquantitativelyanalyzeinvivoabnormalitiesofbiochemicalmetabolismwithinbraintissueinanoninvasiveandnon-radioactivemanner.Comparedwith3.0Tmagneticresonancespectroscopy,high-fieldmagneticresonancespectroscopy(≥7.0T)exhibitshighspatialresolutionanddensityresolution,microscopicimagingofthelivingbody,andobtainsbothhighscanningresolutionandresultprecisionwithinashorterscantime,thusprovidingahighervalueinclinicaldiagnosis.InarecentstudyreportedintheNeuralRegenerationResearch(Vol.9,No.4,2014),7.0TmagneticresonancespectroscopyshowedthatinthehippocampusofAlzheimer’sdiseaserats,theN-acetylaspartatewavecrestwasreduced,andthecreatineandcholinewavecrestwaselevated.Thisfindingwasfurthersupportedbyhematoxylin-eosinstaining,whichshowedalossofhippocampalneuronsandmoreglialcells.Moreover,electronmicroscopyshowedneuronalshrinkageandmitochondrialrupture,andscanningelectronmicroscopyrevealedsmallsizehippocampalsynapticvesicles,incompletesynapticstructure,andreducednumber.Overall,thesefindingsfromLeiZhangandco-workersfromBeijingTiantanHospitalAffiliatedtoCapitalMedicalUniversityinChinarevealedthat7.0Thigh-feldnuclearmagneticresonancespectroscopydetectedthelesionsandfunctionalchangesinhippocampalneuronsofAlzheimer’sdiseaseratsinvivo,allowingthepossibilityforassessingthesuccessrateandgradingoftheanimalmodelofAlzheimer’sdisease.TheMRIT2-weightedimagesshowednosignificantdifferenceinrats2weeksafterAlzheimer’sdiseasewasinduced.Article:7.0Tnuclearmagneticresonanceevaluationoftheamyloidbeta(1–40)animalmodelofAlzheimer’sdisease:comparisonofcytologyverifcation,byLeiZhang1,ShuaiDong2,GuixiangZhao3,YuMa4(1MRNeuroradiologyRoom,BeijingTiantanHospitalAffliatedtoCapitalMedicalUniversity,Beijing,China;2DepartmentofNeurology,SixthPeople’sHospitalofJinan,Jinan,ShandongProvince,China;3DepartmentofRehabilitationMedicine,SixthPeople’sHospitalofJinan,Jinan,ShandongProvince,China;4TsinghuaUniversityYuquanHospital,Beijing,China)ZhangL,DongS,ZhaoGX,MaY.7.0Tnuclearmagneticresonanceevaluationoftheamyloidbeta(1–40)animalmodelofAlzheimer’sdisease:comparisonofcytologyverification.NeuralRegenRes.2014;9(4):430-435.