Alzheimer's disease (AD) is a typical neurodegenerative disease in central nervous system (CNS). Generally speaking, patients with severe AD are often accompanied with cognitive impairment. Oligodendrocytes (OLs) are myelin-forming cells in CNS, and myelin injury potentially has something to do with the cognitive impairment in AD. Based on the previous experimental studies, it has been recognized that nitric oxide (NO), as a signaling molecule, might have an influence on the axon and myelin by affecting the energy transport mechanism of OLs through monocarboxylate transporter 1 (MCT1). Interestingly, a novel model of cell signaling----axo-myelinic synapse (AMS) has been put forward. In the context of this model, chances are that a new way is established in which NO can influence the pathogenesis of AD by down-regulating the expression of MCT1. As a consequence, it may provide attractive prospective and underlying drug targeting effects for the treatment of AD.

中文翻译：

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一氧化氮可能是通过下调单羧酸盐转运蛋白1导致阿尔茨海默氏病认知障碍的诱发因素。

阿尔茨海默氏病（AD）是中枢神经系统（CNS）中典型的神经退行性疾病。一般而言，重度AD患者常伴有认知障碍。少突胶质细胞（OLs）是中枢神经系统中形成髓鞘的细胞，髓鞘损伤可能与AD的认知障碍有关。根据以前的实验研究，已经认识到一氧化氮（NO）作为信号分子可能通过影响OLs通过单羧酸盐转运蛋白1（MCT1）的能量转运机制而对轴突和髓磷脂产生影响。有趣的是，提出了一种新型的细胞信号转导模型-轴-脊髓神经突触（AMS）。在这种模型的背景下，有可能建立一种新的途径，其中NO可以通过下调MCT1的表达来影响AD的发病机制。