author_facet Zhang, Rui
Liu, Yun
Chen, Yan
Li, Qian
Marshall, Charles
Wu, Ting
Hu, Gang
Xiao, Ming
Zhang, Rui
Liu, Yun
Chen, Yan
Li, Qian
Marshall, Charles
Wu, Ting
Hu, Gang
Xiao, Ming
author Zhang, Rui
Liu, Yun
Chen, Yan
Li, Qian
Marshall, Charles
Wu, Ting
Hu, Gang
Xiao, Ming
spellingShingle Zhang, Rui
Liu, Yun
Chen, Yan
Li, Qian
Marshall, Charles
Wu, Ting
Hu, Gang
Xiao, Ming
CNS Neuroscience & Therapeutics
Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
Pharmacology (medical)
Physiology (medical)
Psychiatry and Mental health
Pharmacology
author_sort zhang, rui
spelling Zhang, Rui Liu, Yun Chen, Yan Li, Qian Marshall, Charles Wu, Ting Hu, Gang Xiao, Ming 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.13194 <jats:title>Abstract</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>As a normal physiological process, sleep has recently been shown to facilitate clearance of macromolecular metabolic wastes from the brain via the glymphatic system. The aim of the present study was to investigate pathophysiological roles of astroglial aquaporin 4 (AQP4), a functional regulator of glymphatic clearance, in a mouse model of chronic sleep disruption (SD).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Adult AQP4 null mice and wild‐type (WT) mice were given 7 days of SD using the improved rotating rod method, and then received behavioral, neuropathological, and neurochemical analyses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Aquaporin 4 deletion resulted in an impairment of glymphatic transport and accumulation of β‐amyloid and Tau proteins in the brain following SD. AQP4 null SD mice exhibited severe activation of microglia, neuroinflammation, and synaptic protein loss in the hippocampus, as well as decreased working memory, compared with WT‐SD mice.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These results demonstrate that AQP4‐mediated glymphatic clearance ameliorates brain impairments caused by abnormal accumulation of metabolic wastes following chronic SD, thus serving as a potential target for sleep‐related disorders.</jats:p></jats:sec> Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption CNS Neuroscience & Therapeutics
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series CNS Neuroscience & Therapeutics
source_id 49
title Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_unstemmed Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_full Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_fullStr Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_full_unstemmed Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_short Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_sort aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
topic Pharmacology (medical)
Physiology (medical)
Psychiatry and Mental health
Pharmacology
url http://dx.doi.org/10.1111/cns.13194
publishDate 2020
physical 228-239
description <jats:title>Abstract</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>As a normal physiological process, sleep has recently been shown to facilitate clearance of macromolecular metabolic wastes from the brain via the glymphatic system. The aim of the present study was to investigate pathophysiological roles of astroglial aquaporin 4 (AQP4), a functional regulator of glymphatic clearance, in a mouse model of chronic sleep disruption (SD).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Adult AQP4 null mice and wild‐type (WT) mice were given 7 days of SD using the improved rotating rod method, and then received behavioral, neuropathological, and neurochemical analyses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Aquaporin 4 deletion resulted in an impairment of glymphatic transport and accumulation of β‐amyloid and Tau proteins in the brain following SD. AQP4 null SD mice exhibited severe activation of microglia, neuroinflammation, and synaptic protein loss in the hippocampus, as well as decreased working memory, compared with WT‐SD mice.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These results demonstrate that AQP4‐mediated glymphatic clearance ameliorates brain impairments caused by abnormal accumulation of metabolic wastes following chronic SD, thus serving as a potential target for sleep‐related disorders.</jats:p></jats:sec>
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author Zhang, Rui, Liu, Yun, Chen, Yan, Li, Qian, Marshall, Charles, Wu, Ting, Hu, Gang, Xiao, Ming
author_facet Zhang, Rui, Liu, Yun, Chen, Yan, Li, Qian, Marshall, Charles, Wu, Ting, Hu, Gang, Xiao, Ming, Zhang, Rui, Liu, Yun, Chen, Yan, Li, Qian, Marshall, Charles, Wu, Ting, Hu, Gang, Xiao, Ming
author_sort zhang, rui
container_issue 2
container_start_page 228
container_title CNS Neuroscience & Therapeutics
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description <jats:title>Abstract</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>As a normal physiological process, sleep has recently been shown to facilitate clearance of macromolecular metabolic wastes from the brain via the glymphatic system. The aim of the present study was to investigate pathophysiological roles of astroglial aquaporin 4 (AQP4), a functional regulator of glymphatic clearance, in a mouse model of chronic sleep disruption (SD).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Adult AQP4 null mice and wild‐type (WT) mice were given 7 days of SD using the improved rotating rod method, and then received behavioral, neuropathological, and neurochemical analyses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Aquaporin 4 deletion resulted in an impairment of glymphatic transport and accumulation of β‐amyloid and Tau proteins in the brain following SD. AQP4 null SD mice exhibited severe activation of microglia, neuroinflammation, and synaptic protein loss in the hippocampus, as well as decreased working memory, compared with WT‐SD mice.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These results demonstrate that AQP4‐mediated glymphatic clearance ameliorates brain impairments caused by abnormal accumulation of metabolic wastes following chronic SD, thus serving as a potential target for sleep‐related disorders.</jats:p></jats:sec>
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spelling Zhang, Rui Liu, Yun Chen, Yan Li, Qian Marshall, Charles Wu, Ting Hu, Gang Xiao, Ming 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.13194 <jats:title>Abstract</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>As a normal physiological process, sleep has recently been shown to facilitate clearance of macromolecular metabolic wastes from the brain via the glymphatic system. The aim of the present study was to investigate pathophysiological roles of astroglial aquaporin 4 (AQP4), a functional regulator of glymphatic clearance, in a mouse model of chronic sleep disruption (SD).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Adult AQP4 null mice and wild‐type (WT) mice were given 7 days of SD using the improved rotating rod method, and then received behavioral, neuropathological, and neurochemical analyses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Aquaporin 4 deletion resulted in an impairment of glymphatic transport and accumulation of β‐amyloid and Tau proteins in the brain following SD. AQP4 null SD mice exhibited severe activation of microglia, neuroinflammation, and synaptic protein loss in the hippocampus, as well as decreased working memory, compared with WT‐SD mice.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These results demonstrate that AQP4‐mediated glymphatic clearance ameliorates brain impairments caused by abnormal accumulation of metabolic wastes following chronic SD, thus serving as a potential target for sleep‐related disorders.</jats:p></jats:sec> Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption CNS Neuroscience & Therapeutics
spellingShingle Zhang, Rui, Liu, Yun, Chen, Yan, Li, Qian, Marshall, Charles, Wu, Ting, Hu, Gang, Xiao, Ming, CNS Neuroscience & Therapeutics, Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption, Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology
title Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_full Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_fullStr Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_full_unstemmed Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_short Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_sort aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
title_unstemmed Aquaporin 4 deletion exacerbates brain impairments in a mouse model of chronic sleep disruption
topic Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology
url http://dx.doi.org/10.1111/cns.13194