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      Structural and functional features of central nervous system lymphatics

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          Abstract

          One of the characteristics of the CNS is the lack of a classical lymphatic drainage system. Although it is now accepted that the CNS undergoes constant immune surveillance that takes place within the meningeal compartment 13 , the mechanisms governing the entrance and exit of immune cells from the CNS remain poorly understood 46 . In searching for T cell gateways into and out of the meninges, we discovered functional lymphatic vessels lining the dural sinuses. These structures express all of the molecular hallmarks of lymphatic endothelial cells, are able to carry both fluid and immune cells from the CSF, and are connected to the deep cervical lymph nodes. The unique location of these vessels may have impeded their discovery to date, thereby contributing to the long-held concept of the absence of lymphatic vasculature in the CNS. The discovery of the CNS lymphatic system may call for a reassessment of basic assumptions in neuroimmunology and shed new light on the etiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.

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          Most cited references 34

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          Sleep drives metabolite clearance from the adult brain.

          The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.
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            Inflammation and Alzheimer's disease.

            Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
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              Inflammation and Alzheimer's disease

               H Akiyama (2000)
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                Author and article information

                Journal
                0410462
                6011
                Nature
                Nature
                Nature
                0028-0836
                1476-4687
                9 July 2015
                01 June 2015
                16 July 2015
                16 January 2016
                : 523
                : 7560
                : 337-341
                Affiliations
                [1 ]Center for Brain Immunology and Glia, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [2 ]Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [3 ]Medical Scientist Training Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [4 ]Beirne B. Carter Center for Immunology Research, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [5 ]Department of Medicine (Division of Allergy), School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [6 ]Department of Microbiology, Immunology, and Cancer Biology, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [7 ]Department of Cell Biology, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [8 ]Department of Pathology (Neuropathology), School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                [9 ]Department of Neurosurgery, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
                Author notes
                [* ]Correspondence to: A.L. ( al2hk@ 123456virginia.edu ) or J.K. ( kipnis@ 123456virginia.edu ); Tel: 001 434-982-3858, Fax: 001 434-982-4380
                Article
                NIHMS674511
                10.1038/nature14432
                4506234
                26030524
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