ALZHEIMER'S DISEASE CLASSES AND CINGULATE REORGANIZATION

海马结构和内嗅觉皮质中的神经元 阿尔茨海默病终末期痴呆患者的持续破坏 键入(DAT)。相反，神经元的范围有很大的不同。 后扣带回皮质退行性变及脑组织沉积 神经原纤维缠结(NFT)和神经炎斑块(NP)。案例可以是 根据表达最多的层(S)分为五组 严重的神经元变性。神经元丢失、发作的层状模式 NFT和NP的病程和沉积情况相似 每节课。有人提议在死后组织中进行实验， 探索这些假说：a)扣带回神经元的板层特异性 退化反映独立的DAT类别和b)在 M受体结合可能与干扰 胆碱能和丘脑皮质的联系以一种类别依赖的方式进行。 这四个实验如下。首先，案例样本： 扣带回皮质的神经元、NFT和NP密度将扩大到75 为了提高这些数据的可靠性，包括确定 每个班级的发病年龄，并确定是否有 一组独特的神经细胞变性病例，主要位于第二层。 第二，已有研究表明丘脑前核团变性。 达特。这些核团投射到扣带回皮质，并具有突触前 羟甲喋呤-M可在大脑皮层识别的M受体 或AF-DX 116结合。因此，这个区域的每一个部分，侧核 并将对内侧枕进行神经元变性和NFT的分析 和NP来确定在每一类 疾病。第三，试点研究表明，一类病例减少了 ~3H-氧-曲莫林-M主要在III-V层，而在3类病例中 在ILIC-VI层中结合大量增加。这些现象 暗示在重组中可能有不同的动力在起作用 不同级别DAT的扣带回皮质。从而约束了 奥曲莫林-M将在至少4类这种疾病中进行分析， 会不会为AF-DX 116结合其中，在未标记的情况下 哌仑西平是突触前M碱类药物的选择性治疗方案 感受器。四、半胱氨酸-3结合的层状分布 将被分析以确定是否存在补偿性变化 胆碱能终末与高亲和力胆碱摄取位点的结合 改变了与毒鼠强的配基结合的几层案例 感受器。来自这些研究的数据将提供关于 DAT的神经病理亚型及其新特点 边缘新皮质区域的受体重组。

Neurons in the hippocampal formation and entorhinal cortex are consistently destroyed in end-stage cases of dementia of the Alzheimer type (DAT). In contrast, there is wide variation in the extent of neuron degeneration in posterior cingulate cortex and in the deposition of neurofibrillary tangles (NFT) and neuritic plaques (NP). Cases can be classified into five groups based on the layer(s) which express the most severe neuron degeneration. The laminar pattern of neuron losses, onset and length of the disease and deposition of NFT and NP are similar for each class. Experiments are proposed in postmortem tissue that will explore these hypotheses: a) laminar specificities in cingulate neuron degeneration reflect independent classes of DAT and b) alterations in muscarinic receptor binding may be associated with disruption of cholinergic and thalamocortical connections in a class-dependent manner. The four experiments are as follows. First, the sample of cases for neuron, NFT and NP densities in cingulate cortex will be expanded to 75 to enhance the reliability of this data, including determination of the age at disease onset for each class, and to determine if there is a unique group of cases with neuron degeneration mainly in layer II. Second, it has been shown that the anterior thalamic nuclei degenerate in DAT. These nuclei project to cingulate cortex and have presynaptic muscarinic receptors that can be identified in cortex with oxotremorine-M or AF-DX 116 binding. Thus, each division of this, the lateral nucleus and the medial pulvinar will be analyzed for neuron degeneration and NFT and NP to determine if there are differences within each class of the disease. Third, pilot studies show that a case from class 1 has reduced 3H-oxotremorine-M mainly in layers III-V, while in a case from class 3 binding is massively increased in layers IlIc-VI. These phenomena suggest that there may be different dynamics at work in reorganization of cingulate cortex in different classes of DAT. Thus binding of oxotremorine-M will be analyzed in at least 4 classes of this disease as will that for AF-DX 116 binding which, in the presence of unlabeled pirenzepine, is a selective protocol for presynaptic muscarinic receptors. Fourth, the laminar distribution of hemicholinium-3 binding will be analyzed to determine if there is a compensatory alteration in binding to high affinity choline uptake sites to cholinergic terminals in the layers of cases which have altered ligand binding to muscarinic receptors. The data from these studies will provide new perspectives on neuropathological subtypes of DAT and characterize new features of receptor reorganization in limbic neocortical areas.