Redox-altered plasticity refers to redox-dependent reversible changes in synaptic plasticity via altering functions of key proteins, such as N-methyl-d-aspartate receptor (NMDAR). Age-related cognitive disorders includes Alzheimer's disease (AD), vascular dementia (VD), and age-associated memory impairment (AAMI). Based on the critical role of NMDAR-dependent long-term potentiation (LTP) in memory, the increase of reactive oxygen species in cognitive disorders, and the sensitivity of NMDAR to the redox status, converging lines have suggested the redox-altered NMDAR-dependent plasticity might underlie the synaptic dysfunctions associated with cognitive disorders. In this review, we summarize the involvement of redox-altered plasticity in cognitive disorders by presenting the available evidence. According to reports from our laboratory and other groups, this “redox-altered plasticity” is more similar to functional changes rather than organic injuries, and strategies targeting redox-altered plasticity using pharmacological agents might reverse synaptic dysfunctions and memory abnormalities in the early stage of cognitive disorders. Targeting redox modifications for NMDARs may serve as a novel therapeutic strategy for memory deficits.

氧化还原改变的可塑性是指通过改变关键蛋白质（例如N-甲基-d-天冬氨酸受体（NMDAR）。年龄相关的认知障碍包括阿尔茨海默氏病（AD），血管性痴呆（VD）和年龄相关的记忆障碍（AAMI）。基于NMDAR依赖性长期增强（LTP）在记忆中的关键作用，认知障碍中活性氧的增加以及NMDAR对氧化还原状态的敏感性，汇合线表明氧化还原改变后的NMDAR依赖性可塑性可能是与认知障碍相关的突触功能障碍的原因。在这篇综述中，我们通过提供现有证据总结了氧化还原改变的可塑性在认知障碍中的作用。根据我们实验室和其他小组的报告，这种“氧化还原改变的可塑性”更类似于功能性变化，而不是器质性损伤，使用药理剂针对氧化还原改变的可塑性的策略可能会逆转认知障碍早期的突触功能障碍和记忆异常。针对NMDARs的靶向氧化还原修饰可作为记忆缺陷的新型治疗策略。