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|Title:||Changes in plasma amyloid beta in a longitudinal study of aging and Alzheimer's disease.||Austin Authors:||Rembach, Alan;Faux, Noel G;Watt, Andrew D;Pertile, Kelly K;Rumble, Rebecca L;Trounson, Brett O;Fowler, Christopher J;Roberts, Blaine R;Perez, Keyla A;Li, Qiao-Xin;Laws, Simon M;Taddei, Kevin;Rainey-Smith, Stephanie R;Robertson, Joanne S;Vandijck, Manu;Vanderstichele, Hugo;Barnham, Kevin J;Ellis, Kathryn A;Szoeke, Cassandra;Macaulay, S Lance;Rowe, Christopher C ;Villemagne, Victor L ;Ames, David;Martins, Ralph N;Bush, Ashley I;Masters, Colin L||Institutional Author:||AIBL research group||Affiliation:||National Ageing Research Institute, Parkville, Victoria, Australia
Sir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital), Perth, Western Australia, Australia
Department of Diagnostic Development, Innogenetics NV, Ghent, Belgium
Biomarkable, Gent, Belgium.
Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia
CSIRO Molecular and Health Technologies, Parkville, Victoria, Australia
Centre of Excellence for Alzheimer's Disease Research & Care, School of Medical Sciences, Edith Cowan University, Joondalup. Western Australia, Australia
Department of Psychiatry, St George's Hospital, University of Melbourne, Victoria, Australia
The Mental Health Research Institute, The University of Melbourne, Victoria, Australia
Department of Diagnostic Development, Innogenetics NV, Ghent, Belgium.
|Issue Date:||13-Mar-2013||Publication information:||Alzheimer's & Dementia : the Journal of the Alzheimer's Association 2013; 10(1): 53-61||Abstract:||A practical biomarker is required to facilitate the preclinical diagnosis of Alzheimer's disease (AD).Plasma amyloid beta (Aβ)1-40, Aβ1-42, Aβn-40, and Aβn-42 peptides were measured at baseline and after 18 months in 771 participants from the Australian Imaging Biomarkers and Lifestyle (AIBL) study of aging. Aβ peptide levels were compared with clinical pathology, neuroimaging and neuropsychological measurements.Although inflammatory and renal function covariates influenced plasma Aβ levels significantly, a decrease in Aβ1-42/Aβ1-40 was observed in patients with AD, and was also inversely correlated with neocortical amyloid burden. During the 18 months, plasma Aβ1-42 decreased in subjects with mild cognitive impairment (MCI) and in those transitioning from healthy to MCI.Our findings are consistent with a number of published plasma Aβ studies and, although the prognostic value of individual measures in any given subject is limited, the diagnostic contribution of plasma Aβ may demonstrate utility when combined with a panel of peripheral biomarkers.||URI:||http://ahro.austin.org.au/austinjspui/handle/1/11706||DOI:||10.1016/j.jalz.2012.12.006||URL:||https://pubmed.ncbi.nlm.nih.gov/23491263||Type:||Journal Article||Subjects:||Alzheimer's disease
Pittsburgh compound B
Positron emission tomography
Aged, 80 and over
Alzheimer Disease.blood.genetics.radionuclide imaging
Mild Cognitive Impairment.blood.radionuclide imaging
|Appears in Collections:||Journal articles|
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