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微探针研究与人类中枢神经系统疾病相关的铝积累。

Microprobe studies of aluminum accumulation in association with human central nervous system disease.

机构信息

Neuropathotogy Division, Mount Sinai School of Medicine, One Gustave L. Levy Place, 10029, New York, New York, USA.

出版信息

Environ Geochem Health. 1990 Mar;12(1-2):97-101. doi: 10.1007/BF01734058.

Abstract

The neurofibrillary tangle, first described by Alzheimer in 1907, along with the senile plaque, represent the two principle neuropathologic lesions identified in the brains of patients with Alzheimer's disease. Aluminum salts inoculated into the central nervous system of certain experimental animals induces neurofilamentous lesions which are similar, but not identical to the neurofibrillary tangles seen in Alzheimer's disease. Although some reports provide evidence of increased amounts of aluminum in the brains of Alzheimer's disease victims, such bulk analysis studies have been difficult to replicate. Over the past several years we have approached this problem using a variety of microprobe techniques in order to determine the distribution of trace elements within individual nerve cells.Using scanning electron microscopy with X-ray spectrometry, we have identified accumulations of aluminum in the neurofibrillary tangle-bearing neurons of cases of Alzheimer's disease. Similar accumulations have been found in the brains of the indigenous natives of Guam who suffer from parkinsonism with dementia and from amyotrophic lateral sclerosis. Recent studies using laser microprobe mass analysis suggest that the predominance of aluminum identified within the parikaryon of neurofibrillary tangle-bearing neurons is located within the neurofibrillary tangle itself. Although this ongoing research still cannot ascribe a causal role for aluminum in the etiology and/or pathogenesis of the neurofibrillary tangle, the data suggest that certain environmental factors related to trace elemental constituents may play an important role in the formation of this type of cellular pathology.

摘要

神经原纤维缠结,由阿尔茨海默于 1907 年首次描述,与老年斑一起,是在阿尔茨海默病患者大脑中发现的两种主要神经病理学病变。铝盐接种到某些实验动物的中枢神经系统中会引起神经丝病变,这些病变与阿尔茨海默病中所见的神经原纤维缠结相似,但不完全相同。尽管一些报告提供了阿尔茨海默病患者大脑中铝含量增加的证据,但这种大量分析研究很难重复。在过去的几年中,我们使用各种微探针技术来解决这个问题,以确定单个神经细胞内微量元素的分布。

通过扫描电子显微镜与 X 射线能谱分析,我们已经在阿尔茨海默病病例的神经原纤维缠结神经元中发现了铝的积累。在关岛的土着居民中也发现了类似的积累,他们患有帕金森病伴痴呆和肌萎缩侧索硬化症。最近使用激光微探针质谱分析的研究表明,在神经原纤维缠结神经元的核周质中鉴定出的铝的优势位于神经原纤维缠结本身内。尽管这项正在进行的研究仍然不能将铝在神经原纤维缠结的病因和/或发病机制中的因果作用归因于,但数据表明,与痕量元素成分相关的某些环境因素可能在这种类型的细胞病理学的形成中发挥重要作用。

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