Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17800
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dc.contributor.authorRainey-Smith, Stephanie R-
dc.contributor.authorMazzucchelli, Gavin N-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorBrown, Belinda M-
dc.contributor.authorPorter, Tenielle-
dc.contributor.authorWeinborn, Michael-
dc.contributor.authorBucks, Romola S-
dc.contributor.authorMilicic, Lidija-
dc.contributor.authorSohrabi, Hamid R-
dc.contributor.authorTaddei, Kevin-
dc.contributor.authorAmes, David-
dc.contributor.authorMaruff, Paul-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorSalvado, Olivier-
dc.contributor.authorMartins, Ralph N-
dc.contributor.authorLaws, Simon M-
dc.date2018-02-26-
dc.date.accessioned2018-05-28T06:13:53Z-
dc.date.available2018-05-28T06:13:53Z-
dc.date.issued2018-02-26-
dc.identifier.citationTranslational psychiatry 2018; 8(1): 47en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17800-
dc.description.abstractThe glymphatic system is postulated to be a mechanism of brain Aβ-amyloid clearance and to be most effective during sleep. Ablation of the astrocytic end-feet expressed water-channel protein, Aquaporin-4, in mice, results in impairment of this clearance mechanism and increased brain Aβ-amyloid deposition, suggesting that Aquaporin-4 plays a pivotal role in glymphatic function. Currently there is a paucity of literature regarding the impact of AQP4 genetic variation on sleep, brain Aβ-amyloid burden and their relationship to each other in humans. To address this a cross-sectional observational study was undertaken in cognitively normal older adults from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study. Genetic variants in AQP4 were investigated with respect to self-reported Pittsburgh Sleep Quality Index sleep parameters, positron emission tomography derived brain Aβ-amyloid burden and whether these genetic variants moderated the sleep-Aβ-amyloid burden relationship. One AQP4 variant, rs72878776, was associated with poorer overall sleep quality, while several SNPs moderated the effect of sleep latency (rs491148, rs9951307, rs7135406, rs3875089, rs151246) and duration (rs72878776, rs491148 and rs2339214) on brain Aβ-amyloid burden. This study suggests that AQP4 genetic variation moderates the relationship between sleep and brain Aβ-amyloid burden, which adds weight to the proposed glymphatic system being a potential Aβ-amyloid clearance mechanism and suggests that AQP4 genetic variation may impair this function. Further, AQP4 genetic variation should be considered when interpreting sleep-Aβ relationships.en
dc.language.isoeng-
dc.titleGenetic variation in Aquaporin-4 moderates the relationship between sleep and brain Aβ-amyloid burden.en
dc.typeJournal Articleen
dc.identifier.journaltitleTranslational psychiatryen
dc.identifier.affiliationCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australiaen
dc.identifier.affiliationCSIRO Health and Biosecurity/Australian e-Health Research Centre, Herston, QLD, Australiaen
dc.identifier.affiliationSir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, WA, Australiaen
dc.identifier.affiliationCollaborative Genomics Group, Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australiaen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment of Nuclear Medicine & Centre for PET, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Psychology and Exercise Science, Murdoch University, Murdoch, WA, Australiaen
dc.identifier.affiliationCo-operative Research Centre for Mental Health, Carlton, Victoria, Australiaen
dc.identifier.affiliationSchool of Psychological Science, University of Western Australia, Crawley, WA, Australiaen
dc.identifier.affiliationDepartment of Biomedical Sciences, Macquarie University, North Ryde, NSW, Australiaen
dc.identifier.affiliationAcademic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew, Victoria, Australiaen
dc.identifier.affiliationNational Ageing Research Institute, Parkville, Victoria, Australiaen
dc.identifier.affiliationCogState Ltd., Melbourne, Victoria, Australiaen
dc.identifier.affiliationSchool of Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, WA, Australiaen
dc.identifier.doi10.1038/s41398-018-0094-xen
dc.type.contentTexten
dc.identifier.orcid0000-0001-5819-3026en
dc.identifier.orcid0000-0001-8017-8682en
dc.identifier.orcid0000-0002-4355-7082en
dc.identifier.orcid0000-0003-3910-2453en
dc.identifier.pubmedid29479071-
dc.type.austinJournal Article-
dc.type.austinReview-
local.name.researcherMasters, Colin L
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptMolecular Imaging and Therapy-
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