Abstract：
Brain aging is characterized by several structural, biochemical and molecular changes which can vary among different individuals and can be influenced by genetic, environmental and lifestyle factors. Accumulation of protein aggregates, altered neurotransmitter composition, low-grade chronic inflammation and prolonged oxidative stress have been shown to contribute to brain tissue damage. Among key metabolic byproducts, advanced glycation end products (AGEs), formed endogenously through non-enzymatic reactions or acquired directly from the diet or other exogenous sources, have been detected to accumulate in brain tissue, exerting detrimental effects on cellular structure and function, contributing to neurodegeneration and cognitive decline. Upon binding to signal transduction receptor RAGE, AGEs can initiate pro-inflammatory pathways, exacerbate oxidative stress and neuroinflammation, thus impairing neuronal function and cognition. AGE-RAGE signaling induces programmed cell death, disrupts the blood-brain barrier and promotes protein aggregation, further compromising brain health. In this review, we investigate the intricate relationship between the AGE-RAGE pathway and brain aging in order to detect affected molecules and potential targets for intervention. Reduction of AGE deposition in brain tissue either through novel pharmacological therapeutics, dietary modifications, and lifestyle changes, shows a great promise in mitigating cognitive decline associated with brain aging.
摘要：
大脑老化的特点是几个结构，生化和分子的变化，可以在不同的个体之间变化，并可能受到遗传的影响，环境和生活方式因素。蛋白质聚集体的积累，改变了神经递质的组成，低度慢性炎症和长期氧化应激已被证明有助于脑组织损伤.在关键的代谢副产物中，糖基化终产物（AGEs），通过非酶反应内源性形成或直接从饮食或其他外源性来源获得，被检测到积聚在脑组织中，对细胞结构和功能产生有害影响，导致神经变性和认知能力下降。与信号转导受体RAGE结合后，AGEs可以启动促炎途径，加剧氧化应激和神经炎症，从而损害神经元功能和认知。AGE-RAGE信号诱导程序性细胞死亡，破坏血脑屏障并促进蛋白质聚集，进一步损害大脑健康。在这次审查中,我们研究了AGE-RAGE通路与脑衰老之间的复杂关系,以检测受影响的分子和潜在的干预靶点.通过新的药理疗法减少脑组织中的AGE沉积，饮食调整，生活方式的改变，在减轻与大脑衰老相关的认知能力下降方面显示出巨大的希望。
