Provincial University Key Laboratory of Sport and Health Science, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian, China.
Central Laboratory, Affiliated Fuzhou First Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Int J Biol Sci. 2022 Jan 24;18(4):1569-1579. doi: 10.7150/ijbs.55419. eCollection 2022.
Imbalance of Aβ and tau protein production and clearance are the key factors among many causes of Alzheimer's disease that leading to neurons degeneration and cognitive disorders. As a novel approach, glymphatic system quickly clear metabolic waste (especially Aβ and tau) from cerebral environment, and dysfunction of glymphatic system may relate to occurrence of Alzheimer's disease. Microinfarct is a common histopathologic situation occurring in aging brain and leads to dramatic increase the generation of metabolic by-product after neuronal injury, hindering the operation of glymphatic system and suppress cerebral spinal fluid (CSF) and cerebral interstitial fluid (interstitial fluid, ISF) exchange. Microinfarcts destruct the integrity of microvascular and microstructural tissue, result in Aβ deposition and tau phosphorylation that form neurofibrillary tangles and associated with the cause of Alzheimer's disease. Currently, it has been found that glymphatic system is involved in the pathological process of Alzheimer's disease. Improving the function of glymphatic system after cerebral microinfarcts could be developed as a new approach for Alzheimer's disease prevention and treatment. In this review, we will provide in-depth discussion on functional changes of glymphatic system after cerebral microinfarcts, further reveal pathogenesis of Alzheimer's disease and provide a potentially more effective method for treatment of Alzheimer's disease.
Aβ和 tau 蛋白的产生和清除失衡是导致阿尔茨海默病神经元退化和认知障碍的许多原因中的关键因素。作为一种新方法,糖基化系统可以迅速清除大脑环境中的代谢废物(特别是 Aβ 和 tau),而糖基化系统的功能障碍可能与阿尔茨海默病的发生有关。微梗死是衰老大脑中常见的组织病理学情况,会导致神经元损伤后代谢副产物的大量产生,从而阻碍糖基化系统的运作,并抑制脑脊液(CSF)和脑间质液(间质液,ISF)的交换。微梗死破坏了微血管和微结构组织的完整性,导致 Aβ 沉积和 tau 磷酸化,形成神经原纤维缠结,并与阿尔茨海默病的病因有关。目前,已经发现糖基化系统参与了阿尔茨海默病的病理过程。改善脑微梗死后糖基化系统的功能可能成为预防和治疗阿尔茨海默病的新方法。在这篇综述中,我们将深入讨论脑微梗死后糖基化系统的功能变化,进一步揭示阿尔茨海默病的发病机制,并为阿尔茨海默病的治疗提供一种更有效的潜在方法。