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脑白质疏松症中非共价连接减少。

Reduced noncovalent connections in leukoaraiosis.

作者信息

Szolnoki Zoltán

机构信息

Department of Neurology & Neurophysiology, Pándy Kálmán County Hospital, Gyula, Hungary.

出版信息

Expert Rev Neurother. 2008 Feb;8(2):205-13. doi: 10.1586/14737175.8.2.205.

DOI:10.1586/14737175.8.2.205
PMID:18271708
Abstract

Leukoaraiosis is manifested as diffuse areas of hypodensity on CT scans and as hyperintensity signals on T2-weighted MRI scans. This neuroimaging phenomenon is frequently associated with cognitive decline in the middle-aged or elderly. Ischemic demyelinization or chronic perivascular toxic edema in the white matter of the brain is presumed to be behind this entity. Genetic and environmental factors together lead to the development of leukoaraiosis. The possibility of hypoxia-induced cytoskeleton damage was suggested by recent experimental genetic data. This article discusses the chemical and biochemical consequences of this possibility. It suggests a new approach to leukoaraiosis by linking genetic data, medicinal chemistry, system theory and histopathological data. In accordance with this chemical model, a synchronously evolving slight intracellular ATP depletion along the glial cytoplasm may lead to an unstable biochemical condition in glial cells, which finally predisposes to leukoaraiosis.

摘要

脑白质疏松症在CT扫描上表现为低密度弥漫区域,在T2加权磁共振成像扫描上表现为高信号。这种神经影像学现象常与中老年人的认知衰退相关。脑白质的缺血性脱髓鞘或慢性血管周围中毒性水肿被认为是该病症的病因。遗传和环境因素共同导致脑白质疏松症的发生。近期的实验遗传学数据提示了缺氧诱导细胞骨架损伤的可能性。本文讨论了这种可能性的化学和生化后果。它通过将遗传数据、药物化学、系统理论和组织病理学数据联系起来,提出了一种针对脑白质疏松症的新方法。根据这个化学模型,沿着神经胶质细胞质同步发展的轻微细胞内ATP消耗可能导致神经胶质细胞内不稳定的生化状态,最终易引发脑白质疏松症。

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