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P物质与生长抑素在神经炎性斑块中共存:对阿尔茨海默病发病机制的影响。

Substance P and somatostatin coexist within neuritic plaques: implications for the pathogenesis of Alzheimer's disease.

作者信息

Armstrong D M, Benzing W C, Evans J, Terry R D, Shields D, Hansen L A

机构信息

Department of Neurosciences, University of California, San Diego, School of Medicine, La Jolla 92093.

出版信息

Neuroscience. 1989;31(3):663-71. doi: 10.1016/0306-4522(89)90431-4.

Abstract

In recent years the present authors and others have sought to determine the neurochemical composition of the dilated neuronal processes found within neuritic plaques of patients with Alzheimer's disease. To date a number of neurotransmitter and neuropeptide systems have been observed within different plaques, yet at present it is unclear whether individual human plaques contain more than one transmitter substance. In the present study a highly sensitive dual-immunolabeling procedure was employed and it was demonstrated that substance P and somatostatin-immunoreactive profiles coexist within single senile plaques of patients with Alzheimer's disease. Coexistence of somatostatin and substance P immunoreactivity within plaques was observed in the hippocampus and amygdala but not in the neocortex, although the latter region contained plaques within which somatostatin and substance P existed alone. The frequency with which we observed one or more neuropeptide within plaques was relatively low and in fact most plaques contained neither substance P nor somatostatin immunoreactivity. In addition, a large number of swollen peptidergic processes were observed outside of plaques. The significance of these observations with respect to the pathogenesis of Alzheimer's disease is discussed.

摘要

近年来,本文作者及其他研究者试图确定阿尔茨海默病患者神经炎性斑块内扩张的神经元突起的神经化学成分。迄今为止,在不同的斑块中已观察到多种神经递质和神经肽系统,但目前尚不清楚单个人类斑块是否含有一种以上的递质物质。在本研究中,采用了一种高度敏感的双重免疫标记方法,结果表明P物质和生长抑素免疫反应性成分共存于阿尔茨海默病患者的单个老年斑内。在海马体和杏仁核中观察到斑块内生长抑素和P物质免疫反应性共存,但在新皮质中未观察到,尽管后者区域的斑块中生长抑素和P物质单独存在。我们观察到斑块内存在一种或多种神经肽的频率相对较低,事实上,大多数斑块既没有P物质也没有生长抑素免疫反应性。此外,在斑块外观察到大量肿胀的肽能突起。讨论了这些观察结果对阿尔茨海默病发病机制的意义。

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