PDF(Pubmed)
Abstract：
Currently, there is unavailability of disease-modifying medication for Alzheimer\'s disease (AD), a debilitating neurological disorder. The pathogenesis of AD appears to be complex and could be influenced by the glymphatic system present in the central nervous system (CNS). Amyloid-beta (Aβ) and other metabolic wastes are eliminated from the brain interstitium by the glymphatic system, which encompasses perivascular channels and astroglial cells. Dysfunction of the glymphatic system, which could occur due to decreased aquaporin 4 (AQP4) expression, aging-related alterations in the human brain, and sleep disruptions, may contribute to the pathogenesis of AD and also accelerate the development of AD by causing a buildup of harmful proteins like Aβ. Promising approaches have been examined for reducing AD pathology, including non-pharmacological therapies that target glymphatic function, like exercise and sleep regulation. In addition, preclinical research has also demonstrated the therapeutic potential of pharmaceutical approaches targeted at augmenting AQP4-mediated glymphatic flow. To identify the precise processes driving glymphatic dysfunction in AD and to find new treatment targets, more research is required. Innovative diagnostic and treatment approaches for AD could be made possible by techniques such as dynamic contrast-enhanced MRI, which promises to evaluate glymphatic function in neurodegenerative diseases. Treatment options for AD and other neurodegenerative diseases may be improved by comprehending and utilizing the glymphatic system\'s function in preserving brain homeostasis and targeting the mechanisms involved in glymphatic functioning. This review intends to enhance the understanding of the complex link between AD and the glymphatic system and focuses on the function of AQP4 channels in promoting waste clearance and fluid exchange.
摘要：
目前,阿尔茨海默病（AD）的疾病改善药物不可用，使人衰弱的神经紊乱.AD的发病机制似乎很复杂，可能受到中枢神经系统（CNS）中存在的淋巴系统的影响。淀粉样蛋白-β（Aβ）和其他代谢废物通过淋巴系统从脑间质中消除，包括血管周围通道和星形胶质细胞。淋巴系统的功能障碍，这可能是由于水通道蛋白4（AQP4）表达降低而发生的，人类大脑中与衰老相关的改变，和睡眠中断，可能有助于AD的发病机理，并通过引起Aβ等有害蛋白的积累来加速AD的发展。已经检查了减少AD病理的有希望的方法，包括针对淋巴淋巴功能的非药物疗法，比如锻炼和睡眠调节。此外,临床前研究也证明了靶向增加AQP4介导的淋巴流的药物方法的治疗潜力.为了确定驱动AD患者淋巴淋巴功能障碍的精确过程，并找到新的治疗靶点，需要更多的研究。通过动态对比增强MRI等技术，可以实现AD的创新诊断和治疗方法。有望评估神经退行性疾病中的淋巴淋巴功能。AD和其他神经退行性疾病的治疗选择可以通过理解和利用糖淋巴系统在保持脑稳态和靶向参与糖淋巴功能的机制方面的功能来改善。这篇综述旨在加深对AD与淋巴系统之间复杂联系的理解，并着重于AQP4通道在促进废物清除和流体交换中的功能。
