Crescenzi Rachelle, DeBrosse Catherine, Nanga Ravi P R, Byrne Matthew D, Krishnamoorthy Guruprasad, D'Aquilla Kevin, Nath Hari, Morales Knashawn H, Iba Michiyo, Hariharan Hari, Lee Virginia M Y, Detre John A, Reddy Ravinder
Department of Biochemistry and Molecular Biophysics (BMB), University of Pennsylvania, Philadelphia, Pennsylvania.
Center for Magnetic Resonance and Optical Imaging (CMROI), University of Pennsylvania, Philadelphia, Pennsylvania.
Hippocampus. 2017 Mar;27(3):285-302. doi: 10.1002/hipo.22693. Epub 2017 Feb 3.
Tauopathies are neurodegenerative disorders characterized by abnormal intracellular aggregates of tau protein, and include Alzheimer's disease, corticobasal degeneration, frontotemporal dementia, and traumatic brain injury. Glutamate metabolism is altered in neurodegenerative disorders manifesting in higher or lower concentrations of glutamate, its transporters or receptors. Previously, glutamate chemical exchange saturation transfer (GluCEST) magnetic resonance imaging (MRI) demonstrated that glutamate levels are reduced in regions of synapse loss in the hippocampus of a mouse model of late-stage tauopathy. We performed a longitudinal GluCEST imaging experiment paired with a cross-sectional study of histologic markers of tauopathy to determine whether (1) early GluCEST changes are associated with synapse loss before volume loss occurs in the hippocampus, and whether (2) subhippocampal dynamics in GluCEST are associated with histopathologic events related to glutamate alterations in tauopathy. Live imaging of the hippocampus in three serial slices was performed without exogenous contrast agents, and subregions were segmented based on a k-means cluster model. Subregions of the hippocampus were analyzed (cornu ammonis CA1, CA3, dentate gyrus DG, and ventricle) in order to associate local MRI-observable changes in glutamate with histological measures of glial cell proliferation (GFAP), synapse density (synaptophysin, VGlut1) and glutamate receptor (NMDA-NR1) levels. Early differences in GluCEST between healthy and tauopathy mice were measured in the CA1 and DG subregions (30% reduction, P ≤ 0.001). Synapse density was also significantly reduced in every subregion of the hippocampus in tauopathy mice by 6 months. Volume was not significantly reduced in any subregion until 13 months. Further, a gradient in glutamate levels was observed in vivo along hippocampal axes that became polarized as tauopathy progressed. Dynamics in hippocampal glutamate levels throughout lifetime were most closely correlated with combined changes in synaptophysin and GFAP, indicating that GluCEST imaging may be a surrogate marker of glutamate concentration in glial cells and at the synaptic level. © 2016 Wiley Periodicals, Inc.
tau蛋白病是一类神经退行性疾病,其特征是tau蛋白在细胞内异常聚集,包括阿尔茨海默病、皮质基底节变性、额颞叶痴呆和创伤性脑损伤。在神经退行性疾病中,谷氨酸代谢会发生改变,表现为谷氨酸及其转运体或受体的浓度升高或降低。此前,谷氨酸化学交换饱和转移(GluCEST)磁共振成像(MRI)显示,在晚期tau蛋白病小鼠模型的海马体中,突触丢失区域的谷氨酸水平降低。我们进行了一项纵向GluCEST成像实验,并结合对tau蛋白病组织学标志物的横断面研究,以确定:(1)早期GluCEST变化是否与海马体体积减少之前的突触丢失有关;以及(2)GluCEST的海马体下动态是否与tau蛋白病中与谷氨酸改变相关的组织病理学事件有关。在不使用外源性造影剂的情况下,对三个连续切片中的海马体进行实时成像,并基于k均值聚类模型对亚区域进行分割。对海马体的亚区域(海马角CA1、CA3、齿状回DG和脑室)进行分析,以便将局部MRI可观察到的谷氨酸变化与胶质细胞增殖(GFAP)、突触密度(突触素、VGlut1)和谷氨酸受体(NMDA-NR1)水平的组织学测量结果相关联。在CA1和DG亚区域测量了健康小鼠和tau蛋白病小鼠之间GluCEST的早期差异(降低30%,P≤0.001)。tau蛋白病小鼠海马体的每个亚区域在6个月时突触密度也显著降低。直到13个月时,任何亚区域的体积都没有显著减少。此外,在体内观察到沿海马体轴的谷氨酸水平梯度,随着tau蛋白病的进展,该梯度会极化。整个生命周期中海马体谷氨酸水平的动态变化与突触素和GFAP的联合变化最密切相关,表明GluCEST成像可能是胶质细胞和突触水平谷氨酸浓度的替代标志物。©2016威利期刊公司