Background: Alzheimer's disease (AD) is pathologically characterized by the abnormal accumulation of Aβ and tau proteins. There has long been a keen interest among researchers in understanding how Aβ and tau are ultimately cleared in the brain. The discovery of this glymphatic system introduced a novel perspective on protein clearance and it gained recognition as one of the major brain clearance pathways for clearing these pathogenic proteins in AD. This finding has sparked interest in exploring the potential contribution of the glymphatic/meningeal lymphatic system in AD. Furthermore, there is a growing emphasis and discussion regarding the possibility that activating the glymphatic/meningeal lymphatic system could serve as a novel therapeutic strategy against AD.
Objectives: Given this current research trend, the primary focus of this comprehensive review is to highlight the role of the glymphatic/meningeal lymphatic system in the pathogenesis of AD. The discussion will encompass future research directions and prospects for treatment in relation to the glymphatic/meningeal lymphatic system.
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http://dx.doi.org/10.1007/s00018-024-05225-z | DOI Listing |
Exp Neurol
January 2025
Department of Neurosurgery, Hangzhou First People's Hospital, Hangzhou, Zhejiang, China. Electronic address:
Subarachnoid hemorrhage (SAH) is a severe neurological condition characterized by high morbidity and mortality. The unfavorable prognosis of SAH is closely associated with early brain injury (EBI) and delayed cerebral ischemia (DCI), wherein thrombin plays a role as part of the secondary injury components following hemorrhage in these two pathological processes. Additionally, thrombin contributes to disruptions in the circulation of cerebrospinal fluid (CSF), thereby giving rise to a spectrum of sequelae following SAH, including cerebral edema, hydrocephalus, cognitive impairments, and depressive symptoms.
View Article and Find Full Text PDFLymphology
October 2024
Department of Surgery, University of Arizona College of Medicine-Tucson, Tucson, Arizona USA.
The brain's lymphatic system is comprised of a glymphatic-meningeal-cervical lymphatic vessel pathway. The study of its mechanism and pathophysiology in neurodegenerative disease has been one of the most exciting topics in basic and translational neuroscience of the last decade. However, while there has been some debate about when the meningeal lymphatics were discovered, it cannot be denied that studies in preclinical models and humans in this century represent a monumental step forward in our understanding of how the brain removes metabolic waste, the role this system plays in neurodegenerative disease, and, most importantly, its potential as a novel therapeutic target.
View Article and Find Full Text PDFJ Neuroinflammation
September 2024
Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, Zhejiang, 310009, China.
Acta Neurochir (Wien)
June 2024
Department of Neurosurgery, Oslo University Hospital - Rikshospitalet, Nydalen, Pb 4950 N-0424, Norway.
The discovery of the glymphatic system has fundamentally altered our comprehension of cerebrospinal fluid transport and the removal of waste from brain metabolism. In the past decade, since its initial characterization, research on the glymphatic system has surged exponentially. Its potential implications for central nervous system disorders have sparked significant interest in the field of neurosurgery.
View Article and Find Full Text PDFCell Mol Life Sci
April 2024
Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Background: Alzheimer's disease (AD) is pathologically characterized by the abnormal accumulation of Aβ and tau proteins. There has long been a keen interest among researchers in understanding how Aβ and tau are ultimately cleared in the brain. The discovery of this glymphatic system introduced a novel perspective on protein clearance and it gained recognition as one of the major brain clearance pathways for clearing these pathogenic proteins in AD.
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