Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16085
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dc.contributor.authorThai, Christine-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorLaws, Simon M-
dc.contributor.authorAmes, David-
dc.contributor.authorEllis, Kathryn A-
dc.contributor.authorRainey-Smith, Stephanie R-
dc.contributor.authorMartins, Ralph N-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorMaruff, Paul-
dc.contributor.authorAustralian Imaging, Biomarkers and Lifestyle (AIBL) Research Group-
dc.date2015-10-02-
dc.date.accessioned2016-07-26T04:12:46Z-
dc.date.available2016-07-26T04:12:46Z-
dc.date.issued2015-10-02-
dc.identifier.citationPLoS One 2016; 10(10): e0139082en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16085-
dc.description.abstractHigh levels of β-amyloid (Aβ) in the brain and carriage of the APOE ε4 allele have each been linked to cognitive impairment in cognitively normal (CN) older adults. However, the relationship between these two biomarkers and cognitive decline is unclear. The aim of this study was to investigate the relationship between cerebral Aβ level, APOE ε4 carrier status, and cognitive decline over 18 months, in 317 cognitively healthy (CN) older adults (47.6% males, 52.4% females) aged between 60 and 89 years (Mean = 69.9, SD = 6.8). Cognition was assessed using the Cogstate Brief Battery (CBB) and the California Verbal Learning Test, Second Edition (CVLT-II). Planned comparisons indicated that CN older adults with high Aβ who were also APOE ε4 carriers demonstrated the most pronounced decline in learning and working memory. In CN older adults who were APOE ε4 non-carriers, high Aβ was unrelated to cognitive decline in learning and working memory. Carriage of APOE ε4 in CN older adults with low Aβ was associated with a significantly increased rate of decline in learning and unexpectedly, improved cognitive performance on measures of verbal episodic memory over 18 months. These results suggest that Aβ and APOE ε4 interact to increase the rate of cognitive decline in CN older adults and provide further support for the use of Aβ and APOE ε4 as biomarkers of early Alzheimer's disease.en
dc.subjectAlzheimer Diseaseen
dc.subjectAmyloid beta-peptidesen
dc.subjectMemory disordersen
dc.subjectApolipoprotein E4en
dc.titleAmyloid-Related memory decline in preclinical Alzheimer's Disease is dependent on APOE ε4 and is detectable over 18-monthsen
dc.typeJournal Articleen
dc.identifier.journaltitlePLoS Oneen
dc.identifier.affiliationAustin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationDepartment of Psychology, RMIT University, Melbourne, Australiaen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment of Neurology, Warren Alpert School of Medicine, Brown University, Providence, Rhode Island,USAen
dc.identifier.affiliationDepartment of Neurology, Rhode Island Hospital, Providence, Rhode Island, USAen
dc.identifier.affiliationDepartment of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationCentre of Excellence for Alzheimer’s Disease Research and Care, Edith Cowan University, Joondalup, Western Australia, Australiaen
dc.identifier.affiliationSir James McCusker Alzheimer’s Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia, Australiaen
dc.identifier.affiliationCo-operative Research Centre for Mental Health, Perth, Western Australia, Australiaen
dc.identifier.affiliationNational Ageing Research Institute, Parkville, Victoria, Australiaen
dc.identifier.affiliationAcademic Unit for Psychiatry of Old Age, St. Vincent’s Health, The University of Melbourne, Kew, Victoria, Australiaen
dc.identifier.affiliationCogstate Ltd., Melbourne, Victoria, Australiaen
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/26430784en
dc.identifier.doi10.1371/journal.pone.0139082en
dc.type.contentTexten
dc.identifier.orcid0000-0003-3910-2453en
dc.type.austinJournal Articleen_US
local.name.researcherMasters, Colin L
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
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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