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Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/18059
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dc.contributor.authorBuckley, Rachel F-
dc.contributor.authorMormino, Elizabeth C-
dc.contributor.authorAmariglio, Rebecca E-
dc.contributor.authorProperzi, Michael J-
dc.contributor.authorRabin, Jennifer S-
dc.contributor.authorLim, Yen Ying-
dc.contributor.authorPapp, Kathryn V-
dc.contributor.authorJacobs, Heidi I L-
dc.contributor.authorBurnham, Samantha-
dc.contributor.authorHanseeuw, Bernard J-
dc.contributor.authorDoré, Vincent-
dc.contributor.authorDobson, Annette-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorWaller, Michael-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorMaruff, Paul-
dc.contributor.authorDonohue, Michael C-
dc.contributor.authorRentz, Dorene M-
dc.contributor.authorKirn, Dylan-
dc.contributor.authorHedden, Trey-
dc.contributor.authorChhatwal, Jasmeer-
dc.contributor.authorSchultz, Aaron P-
dc.contributor.authorJohnson, Keith A-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorSperling, Reisa A-
dc.date2018-05-24-
dc.date.accessioned2018-07-10T06:34:24Z-
dc.date.available2018-07-10T06:34:24Z-
dc.date.issued2018-
dc.identifier.citationAlzheimer's & dementia : the journal of the Alzheimer's Association 2018; 14(9): 1193-1203-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/18059-
dc.description.abstractOur objective was to investigate the effect of sex on cognitive decline within the context of amyloid β (Aβ) burden and apolipoprotein E genotype. We analyzed sex-specific effects on Aβ-positron emission tomography, apolipoprotein, and rates of change on the Preclinical Alzheimer Cognitive Composite-5 across three cohorts, such as the Alzheimer's Disease Neuroimaging Initiative, Australian Imaging, Biomarker and Lifestyle, and Harvard Aging Brain Study (n = 755; clinical dementia rating = 0; age (standard deviation) = 73.6 (6.5); female = 55%). Mixed-effects models of cognitive change by sex, Aβ-positron emission tomography, and apolipoprotein ε4 were examined with quadratic time effects over a median of 4 years of follow-up. Apolipoprotein ε4 prevalence and Aβ burden did not differ by sex. Sex did not directly influence cognitive decline. Females with higher Aβ exhibited faster decline than males. Post hoc contrasts suggested that females who were Aβ and apolipoprotein ε4 positive declined faster than their male counterparts. Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. Our findings suggest that sex may play a modifying role on risk of Alzheimer's disease-related cognitive decline.-
dc.language.isoeng-
dc.subjectAPOE-
dc.subjectAmyloid-
dc.subjectCognitive decline-
dc.subjectGender-
dc.subjectPreclinical Alzheimer's disease-
dc.subjectSex-
dc.titleSex, amyloid, and APOE ε4 and risk of cognitive decline in preclinical Alzheimer's disease: Findings from three well-characterized cohorts.-
dc.typeJournal Article-
dc.identifier.journaltitleAlzheimer's & dementia : the journal of the Alzheimer's Association-
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Heidelberg, Victoria, Australia-
dc.identifier.affiliationMelbourne School of Psychological Science, University of Melbourne, Victoria, Australia-
dc.identifier.affiliationHarvard Aging Brain Study, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA-
dc.identifier.affiliationCenter for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA-
dc.identifier.affiliationDepartment of Neurology, Stanford University, CA, USA-
dc.identifier.affiliationDepartment of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA-
dc.identifier.affiliationDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA-
dc.identifier.affiliationFaculty of Health, Medicine and Life Sciences, School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, Maastricht, The Netherlands-
dc.identifier.affiliationThe Australian eHealth Research Centre, CSIRO Health & Biosecurity, Victoria, Australia-
dc.identifier.affiliationDepartment of Neurology, Cliniques Universitaires Saint-Luc, Institute of Neuroscience, Université Catholique de Louvain, Brussels, Belgium-
dc.identifier.affiliationThe University of Queensland, School of Public Health, Faculty of Medicine, Queensland, Australia-
dc.identifier.affiliationDepartment of Nuclear Medicine and Centre for PET, Austin Health, Victoria, Australia-
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Victoria, Australia-
dc.identifier.affiliationCogstate, Ltd., Australia-
dc.identifier.affiliationDepartment of Neurology, University of Southern California, San Diego, CA, USA-
dc.identifier.doi10.1016/j.jalz.2018.04.010-
dc.identifier.orcid0000-0002-5356-5537-
dc.identifier.orcid0000-0003-3910-2453-
dc.identifier.pubmedid29803541-
dc.type.austinJournal Article-
local.name.researcherDoré, Vincent
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptMolecular Imaging and Therapy-
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