Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12728
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dc.contributor.authorGupta, Veer Ben
dc.contributor.authorWilson, Andrea Cen
dc.contributor.authorBurnham, Samanthaen
dc.contributor.authorHone, Eugeneen
dc.contributor.authorPedrini, Steveen
dc.contributor.authorLaws, Simon Men
dc.contributor.authorLim, Wei Ling Florenceen
dc.contributor.authorRembach, Alanen
dc.contributor.authorRainey-Smith, Stephanie Ren
dc.contributor.authorAmes, Daviden
dc.contributor.authorCobiac, Lynneen
dc.contributor.authorMacaulay, S Lanceen
dc.contributor.authorMasters, Colin Len
dc.contributor.authorRowe, Christopher Cen
dc.contributor.authorBush, Ashley Ien
dc.contributor.authorMartins, Ralph Nen
dc.date.accessioned2015-05-16T02:27:37Z
dc.date.available2015-05-16T02:27:37Z
dc.date.issued2015-02-20en
dc.identifier.citationAlzheimer's Research & Therapy 2015; 7(1): 16en
dc.identifier.govdoc25859282en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12728en
dc.description.abstractAlzheimer's disease (AD) is a growing socioeconomic problem worldwide. Early diagnosis and prevention of this devastating disease have become a research priority. Consequently, the identification of clinically significant and sensitive blood biomarkers for its early detection is very important. Apolipoprotein E (APOE) is a well-known and established genetic risk factor for late-onset AD; however, the impact of the protein level on AD risk is unclear. We assessed the utility of plasma ApoE protein as a potential biomarker of AD in the large, well-characterised Australian Imaging, Biomarkers and Lifestyle Study of Ageing (AIBL) cohort.Total plasma ApoE levels were measured at 18-month follow-up using a commercial bead-based enzyme-linked immunosorbent assay: the Luminex xMAP human apolipoprotein kit. ApoE levels were then analysed between clinical classifications (healthy controls, mild cognitive impairment (MCI) and AD) and correlated with the data available from the AIBL cohort, including but not limited to APOE genotype and cerebral amyloid burden.A significant decrease in ApoE levels was found in the AD group compared with the healthy controls. These results validate previously published ApoE protein levels at baseline obtained using different methodology. ApoE protein levels were also significantly affected, depending on APOE genotypes, with ε2/ε2 having the highest protein levels and ε4/ε4 having the lowest. Plasma ApoE levels were significantly negatively correlated with cerebral amyloid burden as measured by neuroimaging.ApoE is decreased in individuals with AD compared with healthy controls at 18-month follow-up, and this trend is consistent with our results published at baseline. The influence of APOE genotype and sex on the protein levels are also explored. It is clear that ApoE is a strong player in the aetiology of this disease at both the protein and genetic levels.en
dc.language.isoenen
dc.titleFollow-up plasma apolipoprotein E levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL) cohort.en
dc.typeJournal Articleen
dc.identifier.journaltitleAlzheimer's research & therapyen
dc.identifier.affiliationFlorey Institute of Neuroscience and Mental Health, Parkville, VIC 3052 Australiaen
dc.identifier.affiliationDepartment of Nuclear Medicine & Centre for PET, Austin Health, Heidelberg, VIC 3084 Australiaen
dc.identifier.affiliationCentre of Excellence in Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, 6027 Australia ; McCusker Alzheimer's Research Foundation, Hollywood Medical Centre, 85 Monash Avenue, Suite 22, Nedlands, 6009 Australia ; Cooperative Research Centre for Mental Health, Carlton, VIC 3053 Australia ; School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Nedlands, 6009 Australiaen
dc.identifier.affiliationCentre of Excellence in Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, 6027 Australia ; McCusker Alzheimer's Research Foundation, Hollywood Medical Centre, 85 Monash Avenue, Suite 22, Nedlands, 6009 Australiaen
dc.identifier.affiliationCSIRO Computational Informatics, Preventative Health Flagship, 65 Brockway Road, Floreat, 6014 Australiaen
dc.identifier.affiliationCentre of Excellence in Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, 6027 Australia ; McCusker Alzheimer's Research Foundation, Hollywood Medical Centre, 85 Monash Avenue, Suite 22, Nedlands, 6009 Australia ; Cooperative Research Centre for Mental Health, Carlton, VIC 3053 Australiaen
dc.identifier.affiliationAcademic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St Vincent's Aged Psychiatry Service, St George's Hospital, Melbourne, VIC 3065 Australia ; National Ageing Research Institute, Parkville, VIC 3052 Australiaen
dc.identifier.affiliationCSIRO Preventative Health Flagship, Adelaide, SA 5000 Australiaen
dc.identifier.affiliationCSIRO, Parkville, VIC 3052 Australiaen
dc.identifier.affiliationCooperative Research Centre for Mental Health, Carlton, VIC 3053 Australia ; Mental Health Research Institute, The University of Melbourne, Parkville, VIC 3052 Australia ; Centre for Neuroscience, The University of Melbourne, Parkville, VIC 3010 Australiaen
dc.identifier.doi10.1186/s13195-015-0105-6en
dc.description.pages16en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25859282en
dc.contributor.corpauthorAIBL Research Groupen
dc.type.austinJournal Articleen
local.name.researcherMasters, Colin L
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptMolecular Imaging and Therapy-
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