Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16191
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dc.contributor.authorBurnham, Samantha C-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorBaker, David-
dc.contributor.authorBush, Ashley I-
dc.contributor.authorDoecke, James D-
dc.contributor.authorFaux, Noel G-
dc.contributor.authorLaws, Simon M-
dc.contributor.authorMartins, Ralph N-
dc.contributor.authorMaruff, Paul-
dc.contributor.authorMacaulay, S Lance-
dc.contributor.authorRainey-Smith, Stephanie R-
dc.contributor.authorSavage, Greg-
dc.contributor.authorAmes, David-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorWilson, William-
dc.contributor.authorVillemagne, Victor L-
dc.date2016-08-17-
dc.date.accessioned2016-09-06T04:21:19Z-
dc.date.available2016-09-06T04:21:19Z-
dc.date.issued2016-09-13-
dc.identifier.citationNeurology 2016; 87(11): 1093-1101en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16191-
dc.description.abstractObjective: We assessed a blood-based signature, which previously demonstrated high accuracy at stratifying individuals with high or low neocortical β-amyloid burden (NAB), to determine whether it could also identify individuals at risk of progression to Alzheimer disease (AD) within 54 months. Methods: We generated the blood-based signature for 585 healthy controls (HCs) and 74 participants with mild cognitive impairment (MCI) from the Australian Imaging, Biomarkers and Lifestyle Study who underwent clinical reclassification (blinded to biomarker findings) at 54-month follow-up. The individuals were split into estimated high and low NAB groups based on a cutoff of 1.5 standardized uptake value ratio. We assessed the predictive accuracy of the high and low NAB groupings based on progression to mild cognitive impairment or AD according to clinical reclassification at 54-month follow-up. Results: Twelve percent of HCs with estimated high NAB progressed in comparison to 5% of HCs with estimated low NAB (odds ratio = 2.4). Forty percent of the participants with MCI who had estimated high NAB progressed in comparison to 5% of the participants with MCI who had estimated low NAB (odds ratio = 12.3). These ratios are in line with those reported for Pittsburgh compound B–PET results. Individuals with estimated high NAB had faster rates of memory decline than those with estimated low NAB. Conclusion: These findings suggest that a simple blood-based signature not only provides estimates of NAB but also predicts cognitive decline and disease progression, identifying individuals at risk of progressing toward AD at the prodromal and preclinical stages.en
dc.titlePredicting Alzheimer disease from a blood-based biomarker profile: A 54-month follow-upen
dc.typeJournal Articleen
dc.identifier.journaltitleNeurologyen
dc.identifier.affiliationAustin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationeHealth, CSIRO Health and Biosecurity, Floreat, Western Australia, Australiaen
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.affiliationJanssen Research and Development, Titusville, NJ, USAen
dc.identifier.affiliationMental Health Research Institute, Academic Unit for Psychiatry of Old Age, the University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment 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.affiliationeHealth, CSIRO Health and Biosecurity, Herston, Queensland, Australiaen
dc.identifier.affiliationCentre of Excellence for Alzheimer's Disease Research & Care, School of Medical Sciences, Edith Cowan University, Joondalup, Western Australia, Australiaen
dc.identifier.affiliationSchool of Biomedical Sciences, Faculty of Health Sciences, Curtin University, Bentley, Western Australia, Australiaen
dc.identifier.affiliationSir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital), Perth, Western Australia, Australiaen
dc.identifier.affiliationCogstate, Melbourne, Victoria, Australiaen
dc.identifier.affiliationCSIRO Food and Nutrition Flagship, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Psychology, Macquarie University, Sydney, NSW, Australiaen
dc.identifier.affiliationeHealth, CSIRO Health and Biosecurity, North Ryde, NSW, Australiaen
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/27534714en
dc.identifier.doi10.1212/WNL.0000000000003094en
dc.type.contentTexten
dc.identifier.orcid0000-0003-3910-2453en
dc.identifier.orcid0000-0001-8259-9069en
dc.type.austinJournal Articleen_US
local.name.researcherMasters, Colin L
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
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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