Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/22415
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dc.contributor.authorDang, Christa-
dc.contributor.authorYassi, Nawaf-
dc.contributor.authorHarrington, Karra D-
dc.contributor.authorXia, Ying-
dc.contributor.authorLim, Yen Ying-
dc.contributor.authorAmes, David-
dc.contributor.authorLaws, Simon M-
dc.contributor.authorHickey, Martha-
dc.contributor.authorRainey-Smith, Stephanie-
dc.contributor.authorSohrabi, Hamid R-
dc.contributor.authorDoecke, James D-
dc.contributor.authorFripp, Jurgen-
dc.contributor.authorSalvado, Olivier-
dc.contributor.authorSnyder, Peter J-
dc.contributor.authorWeinborn, Michael-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorMaruff, Paul-
dc.date2019-09-12-
dc.date.accessioned2020-01-13T04:06:14Z-
dc.date.available2020-01-13T04:06:14Z-
dc.date.issued2019-12-
dc.identifier.citationAlzheimer's & dementia (Amsterdam, Netherlands) 2019; 11: 566-575en
dc.identifier.issn2352-8729-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/22415-
dc.description.abstractSuperior cognitive performance in older adults may reflect underlying resistance to age-associated neurodegeneration. While elevated amyloid β (Aβ) deposition (Aβ+) has been associated with increased cortical atrophy, it remains unknown whether "SuperAgers" may be protected from Aβ-associated neurodegeneration. Neuropsychologically defined SuperAgers (n = 172) and cognitively normal for age (n = 172) older adults from the Australian Imaging, Biomarkers and Lifestyle study were case matched. Rates of cortical atrophy over 8 years were examined by SuperAger classification and Aβ status. Of the case-matched SuperAgers and cognitively normal for age older adults, 40.7% and 40.1%, respectively, were Aβ+. Rates of age- and Aβ-associated atrophy did not differ between the groups on any measure. Aβ- individuals displayed the slowest rates of atrophy. Maintenance of superior memory in late life does not reflect resistance to age- or Aβ-associated atrophy. However, those individuals who reached old age without cognitive impairment nor elevated Aβ deposition (i.e. Aβ-) displayed reduced rates of cortical atrophy.en
dc.language.isoeng-
dc.subjectAgingen
dc.subjectAlzheimer's diseaseen
dc.subjectMemoryen
dc.subjectNeurodegenerationen
dc.subjectβ-amyloiden
dc.titleRates of age- and amyloid β-associated cortical atrophy in older adults with superior memory performance.en
dc.typeJournal Articleen
dc.identifier.journaltitleAlzheimer's & dementia (Amsterdam, Netherlands)en
dc.identifier.affiliationNational Ageing Research Institute, Parkville, Victoria, Australiaen
dc.identifier.affiliationCollaborative Genomics Group, Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Perth, Western Australia, Australiaen
dc.identifier.affiliationSchool of Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australiaen
dc.identifier.affiliationAcademic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationCSIRO Health and Biosecurity, the Australian eHealth Research Centre, Brisbane, Queensland, Australiaen
dc.identifier.affiliationCooperative Research Centre for Mental Health, Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine and Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Obstetrics and Gynaecology, Melbourne Medical School, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationCentre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Perth, Western Australia, Australiaen
dc.identifier.affiliationAustralian Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia, Australiaen
dc.identifier.affiliationSchool of Psychological Science, University of Western Australia, Crawley, Western Australia, Australiaen
dc.identifier.affiliationSchool of Psychiatry and Clinical Neurosciences, University of Western Australia, Nedlands, Western Australia, Australiaen
dc.identifier.affiliationCogState Ltd., Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Molecular Imaging & Therapy, Austin Health, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationGeorge & Anne Ryan Institute for Neuroscience, The University of Rhode Island, Kingston, RI, USAen
dc.identifier.doi10.1016/j.dadm.2019.05.005en
dc.type.contentTexten
dc.identifier.orcid0000-0003-3910-2453en
dc.identifier.pubmedid31909172-
dc.type.austinJournal Article-
local.name.researcherMasters, Colin L
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.deptMolecular Imaging and Therapy-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
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