A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort

Abstract Alzheimer’s Disease (AD) is the most common form of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofibrillary tangles of tau protein. As no current clinical test can diagnose individuals at risk of developing AD, the aim of this project is to e...

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Autores principales:	Steve Pedrini, Veer B. Gupta, Eugene Hone, James Doecke, Sid O’Bryant, Ian James, Ashley I. Bush, Christopher C. Rowe, Victor L. Villemagne, David Ames, Colin L. Masters, Ralph N. Martins, AIBL Research Group
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/28c8e933dd1349c98d3838986758d187
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spelling	oai:doaj.org-article:28c8e933dd1349c98d3838986758d1872021-12-02T15:05:21ZA blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort10.1038/s41598-017-14020-92045-2322https://doaj.org/article/28c8e933dd1349c98d3838986758d1872017-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-14020-9https://doaj.org/toc/2045-2322Abstract Alzheimer’s Disease (AD) is the most common form of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofibrillary tangles of tau protein. As no current clinical test can diagnose individuals at risk of developing AD, the aim of this project is to evaluate a blood-based biomarker panel to identify individuals who carry this risk. We analysed the levels of 22 biomarkers in clinically classified healthy controls (HC), mild cognitive impairment (MCI) and Alzheimer’s participants from the well characterised Australian Imaging, Biomarker and Lifestyle (AIBL) study of aging. High levels of IL-10 and IL-12/23p40 were significantly associated with amyloid deposition in HC, suggesting that these two biomarkers might be used to detect at risk individuals. Additionally, other biomarkers (Eotaxin-3, Leptin, PYY) exhibited altered levels in AD participants possessing the APOE ε4 allele. This suggests that the physiology of some potential biomarkers may be altered in AD due to the APOE ε4 allele, a major risk factor for AD. Taken together, these data highlight several potential biomarkers that can be used in a blood-based panel to allow earlier identification of individuals at risk of developing AD and/or early stage AD for which current therapies may be more beneficial.Steve PedriniVeer B. GuptaEugene HoneJames DoeckeSid O’BryantIan JamesAshley I. BushChristopher C. RoweVictor L. VillemagneDavid AmesColin L. MastersRalph N. MartinsAIBL Research GroupNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Steve Pedrini Veer B. Gupta Eugene Hone James Doecke Sid O’Bryant Ian James Ashley I. Bush Christopher C. Rowe Victor L. Villemagne David Ames Colin L. Masters Ralph N. Martins AIBL Research Group A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
description	Abstract Alzheimer’s Disease (AD) is the most common form of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofibrillary tangles of tau protein. As no current clinical test can diagnose individuals at risk of developing AD, the aim of this project is to evaluate a blood-based biomarker panel to identify individuals who carry this risk. We analysed the levels of 22 biomarkers in clinically classified healthy controls (HC), mild cognitive impairment (MCI) and Alzheimer’s participants from the well characterised Australian Imaging, Biomarker and Lifestyle (AIBL) study of aging. High levels of IL-10 and IL-12/23p40 were significantly associated with amyloid deposition in HC, suggesting that these two biomarkers might be used to detect at risk individuals. Additionally, other biomarkers (Eotaxin-3, Leptin, PYY) exhibited altered levels in AD participants possessing the APOE ε4 allele. This suggests that the physiology of some potential biomarkers may be altered in AD due to the APOE ε4 allele, a major risk factor for AD. Taken together, these data highlight several potential biomarkers that can be used in a blood-based panel to allow earlier identification of individuals at risk of developing AD and/or early stage AD for which current therapies may be more beneficial.
format	article
author	Steve Pedrini Veer B. Gupta Eugene Hone James Doecke Sid O’Bryant Ian James Ashley I. Bush Christopher C. Rowe Victor L. Villemagne David Ames Colin L. Masters Ralph N. Martins AIBL Research Group
author_facet	Steve Pedrini Veer B. Gupta Eugene Hone James Doecke Sid O’Bryant Ian James Ashley I. Bush Christopher C. Rowe Victor L. Villemagne David Ames Colin L. Masters Ralph N. Martins AIBL Research Group
author_sort	Steve Pedrini
title	A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
title_short	A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
title_full	A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
title_fullStr	A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
title_full_unstemmed	A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort
title_sort	blood-based biomarker panel indicates il-10 and il-12/23p40 are jointly associated as predictors of β-amyloid load in an ad cohort
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/28c8e933dd1349c98d3838986758d187
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A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort

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