多发性硬化的病因学

E. Lundsgaard
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引用次数: 0

摘要

多发性硬化症(MS)的特征是中枢神经系统(CNS)白质中神经周围的髓鞘退化。我认为这是由于髓磷脂产生不足引起的,因为形成髓磷脂的少突胶质细胞受到细胞质中过量的1型类固醇受体的损伤,由于配体的相对缺乏,这些受体聚集并释放锌。这可能逐渐导致tau蛋白的过度磷酸化。因此,多发性硬化症的病因基础被认为是至少三个协同系统与成分,类固醇受体1型及其配体:维生素D,雌激素和睾酮。为了证明这个有许多变量的假设,必须使用一个非齐次微分方程系统。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Etiology of Multiple Sclerosis
Multiple Sclerosis (MS) is characterized by degradation of the essential myelin sheath around the nerves in the white matter of the central nervous system (CNS). I argue that this is caused by insufficient production of myelin, as myelin-forming oligodendrocytes become damaged by excess steroid receptors type 1 in the cytoplasm, which clump and release zinc due to the relative lack of their ligands. This may gradually lead to hyperphosphorylation of tau protein. Accordingly, the etiological basis for MS is thought to be at least three synergistic systems with the components, steroid receptors type 1 and their ligands: vitamin D, estrogen and testosterone. To prove this hypothesis with its many variables, it has been necessary to use a system of non-homogeneous differential equations.
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