Seattle Science Foundation, Seattle, Washington.
Swedish Neuroscience Institute, Swedish Medical Center, Seattle, Washington.
Lymphat Res Biol. 2020 Feb;18(1):2-6. doi: 10.1089/lrb.2018.0079. Epub 2019 Aug 21.
Alzheimer's disease (AD) is a complex neurodegenerative disorder causing progressive cognitive decline, memory loss, and death of neural tissue. Current research suggests a connection between bulk flow of interstitial fluid and cerebrospinal fluid across the blood-brain barrier and the recently confirmed meningeal lymphatic channels of the brain. The main symptom of interest in AD is the spontaneous aggregation of amyloid beta (Aβ) proteins resulting from increased production or lack of clearance from brain tissues. These protein aggregates manifest as plaques in the capillary and artery lumina and the neuronal and dural tissues of the brain, and are known to contribute to cerebral amyloid angiopathy and a host of other neuroinflammatory conditions. The meningeal lymphatics contain a substantial population of immune cells and also serve as a drain into the deep cervical lymph nodes. In this study we discuss the molecular mechanisms by which Aβ could gain access to meningeal lymphatic channels through the blood-brain interface, including ways in which it can be cleared to preclude aggregation and plaque deposition.
阿尔茨海默病(AD)是一种复杂的神经退行性疾病,导致进行性认知能力下降、记忆力丧失和神经组织死亡。目前的研究表明,细胞间质液和脑脊液在血脑屏障中的体循环与最近证实的脑脑膜淋巴管之间存在联系。AD 中感兴趣的主要症状是淀粉样β(Aβ)蛋白的自发聚集,这是由于脑组织中产生增加或清除减少所致。这些蛋白聚集体表现为毛细血管和动脉管腔以及脑的神经元和硬脑膜组织中的斑块,已知会导致脑淀粉样血管病和许多其他神经炎症状况。脑膜淋巴管中含有大量的免疫细胞,也是进入深部颈淋巴结的引流途径。在这项研究中,我们讨论了 Aβ 通过血脑界面进入脑膜淋巴管的分子机制,包括可以清除以防止聚集和斑块沉积的方法。