Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging Christopher C. Rowe a, *, Kathryn A. Ellis b,c,d , Miroslava Rimajova e , Pierrick Bourgeat f , Kerryn E. Pike a , Gareth Jones a , Jurgen Fripp f , Henri Tochon-Danguy a , Laurence Morandeau g , Graeme O’Keefe a , Roger Price g , Parnesh Raniga f , Peter Robins g , Oscar Acosta f , Nat Lenzo e , Cassandra Szoeke h , Olivier Salvado f , Richard Head h , Ralph Martins e , Colin L. Masters c , David Ames d , Victor L. Villemagne a,c a Austin Health, Department of Nuclear Medicine and Centre for PET, Heidelberg, Victoria,Australia b University of Melbourne, Department of Psychiatry, Parkville, Australia c The Mental Health Research Institute, Parkville, Victoria, Australia d National Ageing Research Institute, Parkville, Victoria, Australia e Edith Cowan University, School of Exercise, Biomedical and Health Sciences, Joondalup, Western Australia, Australia f CSIRO Preventative Health National Research Flagship, The Australian e-Health Research Centre - BioMedIA, Herston, Queensland, Australia g WA PET and Cyclotron Service, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia h CSIRO Preventative Health Flagship, Parkville, Victoria, Australia Received 17 February 2010; received in revised form 1 April 2010; accepted 5 April 2010 Abstract The Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging, a participant of the worldwide Alzheimer’s Disease Neuroimaging Initiative (ADNI), performed 11 C-Pittsburgh Compound B (PiB) scans in 177 healthy controls (HC), 57 mild cognitive impairment (MCI) subjects, and 53 mild Alzheimer’s disease (AD) patients. High PiB binding was present in 33% of HC (49% in ApoE-4 carriers vs 21% in noncarriers) and increased with age, most strongly in 4 carriers. 18% of HC aged 60-69 had high PiB binding rising to 65% in those over 80 years. Subjective memory complaint was only associated with elevated PiB binding in 4 carriers. There was no correlation with cognition in HC or MCI. PiB binding in AD was unrelated to age, hippocampal volume or memory. Beta-amyloid (A) deposition seems almost inevitable with advanced age, amyloid burden is similar at all ages in AD, and secondary factors or downstream events appear to play a more direct role than total beta amyloid burden in hippocampal atrophy and cognitive decline. Crown Copyright © 2010 Published by Elsevier Inc. All rights reserved. Keywords: Alzheimer’s disease; Mild cognitive impairment; Amyloid imaging; Positron emission tomography; Magnetic resonance imaging 1. Introduction Dementia is a leading cause of death, disability, and health expenditure in the elderly and Alzheimer’s disease (AD) accounts for the majority of cases. The leading hy- pothesis on the cause of AD is that it results from excessive beta amyloid (A) in the brain, either through increased production or impaired clearance of A oligomers that then aggregate to form extracellular plaques and vascular wall deposits (Villemagne et al., 2006). However, there are many unanswered questions regarding this hypothesis including the timing and rate of A deposition and its relationship to brain atrophy and cognitive decline. * Corresponding author at: Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road, Heidelberg, Vic. 3084, Australia. Tel: +61 3 9496 5183. E-mail address: Christopher.Rowe@austin.org.au (C. Rowe). Neurobiology of Aging 31 (2010) 1275–1283 www.elsevier.com/locate/neuaging 0197-4580/$ – see front matter Crown Copyright © 2010 Published by Elsevier Inc. All rights reserved. doi:10.1016/j.neurobiolaging.2010.04.007