Reactive oxygen species (ROS) are metabolic byproducts that are necessary for physiological function but can be toxic at high levels. Levels of these oxidative stressors increase gradually throughout the lifespan, impairing mitochondrial function and damaging all parts of the body, particularly the central nervous system. Emerging evidence suggests that accumulated oxidative stress may be one of the key mechanisms causing cognitive aging and neurodegenerative diseases such as Alzheimer's disease (AD). Here, we synthesize the current literature on the effect of neuronal oxidative stress on mitochondrial dysfunction, DNA damage and epigenetic changes related to cognitive aging and AD. We further describe how oxidative stress therapeutics such as antioxidants, caloric restriction and physical activity can reduce oxidation and prevent cognitive decline in brain aging and AD. Of the currently available therapeutics, we propose that long term physical activity is the most promising avenue for improving cognitive health by reducing ROS while promoting the low levels required for optimal function.

活性氧 (ROS) 是生理功能所必需的代谢副产物，但在高水平时可能有毒。这些氧化应激物的水平在整个生命周期中逐渐增加，损害线粒体功能并损害身体的所有部位，特别是中枢神经系统。新出现的证据表明，累积的氧化应激可能是导致认知老化和阿尔茨海默病 (AD) 等神经退行性疾病的关键机制之一。在这里，我们综合了当前关于神经元氧化应激对线粒体功能障碍、DNA 损伤以及与认知老化和 AD 相关的表观遗传变化影响的文献。我们进一步描述了氧化应激疗法如抗氧化剂如何，热量限制和身体活动可以减少氧化并防止大脑衰老和 AD 的认知能力下降。在目前可用的治疗方法中，我们建议长期体育活动是通过减少活性氧同时促进最佳功能所需的低水平来改善认知健康的最有希望的途径。