Nitric oxide might be an inducing factor in cognitive impairment in Alzheimer's disease via downregulating the monocarboxylate transporter 1.

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.