PATHOLOGY OF FASCIA DENTATA IN ALZHEIMERS DISEASE

神经炎性斑块是阿尔茨海默病和正常衰老的关键特征。 海马结构内的神经炎斑块具有非常特征性的 分布在分子层的筋膜齿，在那里他们是 与颗粒细胞层平行排列。 这种精确的预测 模式提供了一个独特的机会，以确定斑块定位， 传入分子层的分布和 颗粒细胞树突形态。 两组实验将测试 这一假说认为，传入神经分布的变化和 颗粒细胞的形态随着第一个噬斑的出现而发展。 的 第三组实验将检查小胶质细胞和淀粉样蛋白在 斑块形成在这个明确界定的神经炎斑块群体中。 的 这些实验的最终目标是开发分子层， 筋膜作为一个模型系统，其中检查的发病机制， 阿尔茨海默病的神经炎斑块 首先，在控制和 老年痴呆症患者将与层状分布有关 神经炎斑块 每个Rapid将使用多个解剖标记 尸检案。 内嗅皮层的穿通路径 用荧光染料Dil标记。 胆碱能传入神经 基底前脑胆碱能核将用 乙酰胆碱酯酶组织化学 生长抑素和胆囊收缩素 传入神经将被化学标记。第二，关系 将确定神经纤维素斑块和颗粒细胞之间的关系。 细胞内注射荧光黄会填满树突树， 树突的分支模式和树突的病理学是有关联的 斑块的位置。 异常颗粒细胞体的分布 含有神经纤维缠结的匹克样小体，或异常 神经丝抗原将与斑块的分布相关 在上面的分子层中。 第三，积累模式 小胶质细胞和淀粉样蛋白将与神经元中的上述变化相关， RCA-1凝集素组化标记小胶质细胞，刚果红染色 和淀粉样β蛋白免疫组织化学标记淀粉样蛋白。 淀粉样 沉积也将与痴呆发作的年龄相关， 痴呆持续时间和痴呆家族史。

Neuritic plaques are a key feature of Alzheimer's disease and normal aging. Neuritic plaque within the hippocampal formation have a very characteristic distribution in the molecular layer of the fascia dentata, where they are aligned parallel to the granule cell layer. This precise predictable pattern provides a unique opportunity to define plaque localization in terms of both the distribution of afferents to the molecular layer and the morphology of granule cell dendrites. Two sets of experiments will test the hypothesis that changes in the distribution of afferents and change in the morphology of granule cells develop as the first plaques appear. The third set of experiment will examine the role of microglia and amyloid in plaque formation in this well-defined population of neuritic plaques. The ultimate goal of these experiments is to develop the molecular layer of the fascia dentata as a model system in which to examine the pathogenesis of neuritic plaques in Alzheimer's disease. First, the distribution of afferents to the molecular layer in control and Alzheimer's disease patients will be related to the laminar distribution of neuritic plaques. Multiple anatomic marker will be used in each Rapid Autopsy case. The perforant path from the entorhinal cortex will be labeled with the fluorescent dye Dil. The cholinergic afferents from the basal forebrain cholinergic nuclei will be labeled with acetylcholinesterase histochemistry. Somatostatin and cholecystokinin afferents will be labeled immunohistochemically. Second, the relationships between the neuritin plaques and the granule cells will be defined. Intracellular injections of Lucifer yellow will fill the dendritic trees so that dendritic branching patterns and dendritic pathology can be correlated with plaque location. The distribution of abnormal granule cell bodies containing neurofibrillary tangles Pick-like bodies, or abnormal neurofilament antigens will be correlated with the distribution of plaques in the overlying molecular layer. Third, patterns of accumulation of microglia and amyloid will be related to the above changes in the neuropil, using RCA-1 lectin histochemistry to label microglia and Congo red staining and amyloid beta protein immunohistochemistry to label amyloid. Amyloid deposition will also be correlated with the age of onset of dementia, duration of dementia and family history of dementia.