1H MRSI AND PERFUSION MRI OF SIVD

简单地说，这个项目的结果（总共120名受试者，分为6组，每组20人）是：1。与老年对照组（CN）相比，具有腔隙的痴呆患者（D）（+L，其中许多人患有皮质下缺血性血管性痴呆（SIVD））的皮质灰质（CGM）和海马体中的N-乙酰天冬氨酸[NAA]减少，与无腔隙的D（其中许多人患有阿尔茨海默病）的变化相似。2)与非丘脑L型相比，丘脑腔隙型患者的额叶cGM [NAA]降低。3)CGM [NAA]与L数量和白色病变（WML）%成比例降低。4)MMSE和特定神经心理学测试与CGM [NAA]相关。综上所述，这些发现强烈支持D组CGM [NAA]降低的观点，并且这种降低在程度和位置上与皮质下梗死成比例。我们将CGM[NAA]降低解释为皮质下梗死导致损伤、体积缩小或数量减少，或皮质神经元减少。本项目将通过使用短TE 1H MRSI测量肌醇（阿尔茨海默病的假定标记物）和使用动脉自旋标记灌注MRI定量皮质和皮质下灌注来扩展这些发现。样本量约为60例受试者/组，随后进行尸检，以进行阿尔茨海默病和/或梗死的最终病理诊断。所有受试者都将接受MRI分割和海马体积测量，以及多层短TE 1H MRSI。其他相关目标是：1.）确定SIVD和AD中NAA、肌醇和灌注改变的相对程度。2.）确定皮质下梗死和皮质神经元损伤在痴呆中的相对程度。3.）第三章开发可靠区分SIVD和AD的死前分类方法。4.）建立SIVD和AD认知功能下降的可靠产品。该项目将有助于确定皮质下梗死对认知的影响，预测皮质下梗死对认知能力下降的影响，并有助于区分SIVD和AD。其意义在于，这项工作将提供有关SIVD和AD的发病机制的新认识，提高这两种疾病的生前诊断，并提供评价临床治疗试验结果的方法。

Briefly, the findings of this project (total of 120 subjects, divided into 6 groups of 20 each) were: 1.) Reduced N-acetyl aspartate [NAA] in cortical gray matter (cGM) and hippocampus of demented patients (D) with lacunes (+L many of whom have subcortical ischemic vascular dementia (SIVD)) compared to elderly controls (CN), similar to changes in D without lacunes (many of whom have Alzheimer's). 2) Frontal cGM [NAA] was reduced to patients with thalamic lacunes, compared to those with non thalamic L. 3) cGM [NAA] was reduced in proportion to number of L and to % white matter lesions (WML). 4) MMSE and specific neuropsychological tests correlated with cGM [NAA]. Taken together, these finding strongly support the view that cGM [NAA] is reduced in D, and that this reduction is proportional in extent and location to subcortical infarction. We interpret the reduced cGM[NAA] to indicate either injury, reduced size, or reduced number, or cortical neurons, in response to subcortical infarction. This project will extend these findings by using short TE 1H MRSI to measure myo-inositol (a putative marker of Alzheimer's disease) and by using arterial spin labeled perfusion MRI to quantitate cortical and subcortical perfusion. The sample size will be about 60 subjects/group, followed autopsy for final pathological diagnosis of Alzheimer's and/or infarction. All subjects will have MRI with segmentation and hippocampal voluming, and multi-slice short TE 1H MRSI. Other related goals are to: 1.) Determine the relative extent that NAA, myoinositol, and perfusion are altered in SIVD and AD. 2.) To determine the relative extent to which subcortical infarction and cortical neuron damage contribute to dementia. 3.) To develop antemortem classification methods which reliably distinguish between SIVD and AD. 4.) To establish reliable products of cognitive decline in SIVD and AD. This project will help determine the effects of subcortical infarction on cognition, predict the effects of subcortical infarction our cognitive decline, and help distinguish between SIVD and AD. The significance is that this work will provide new understanding concerning the pathogenesis of SIVD and AD, improve the antemortem diagnosis of both disorders, and provide methods for evaluation the results of clinical treatment trials.