Journal article
Impact of APOE-epsilon 4 carriage on the onset and rates of neocortical A beta-amyloid deposition
Samantha C Burnham, Simon M Laws, Charley A Budgeon, Vincent Dore, Tenielle Porter, Pierrick Bourgeat, Rachel F Buckley, Kevin Murray, Kathryn A Ellis, Berwin A Turlach, Olivier Salvado, David Ames, Ralph N Martins, Dorene Rentz, Colin L Masters, Christopher C Rowe, Victor L Villemagne
Neurobiology of Aging | ELSEVIER SCIENCE INC | Published : 2020
Abstract
Neocortical Aβ-amyloid deposition, one of the hallmark pathologic features of Alzheimer's disease (AD), begins decades prior to the presence of clinical symptoms. As clinical trials move to secondary and even primary prevention, understanding the rates of neocortical Aβ-amyloid deposition and the age at which Aβ-amyloid deposition becomes abnormal is crucial for optimizing the timing of these trials. As APOE-ε4 carriage is thought to modulate the age of clinical onset, it is also important to understand the impact of APOE-ε4 carriage on the age at which the neocortical Aβ-amyloid deposition becomes abnormal. Here, we show that, for 455 participants with over 3 years of follow-up, abnormal le..
View full abstractGrants
Awarded by NHMRC
Awarded by ADNI (National Institutes of Health)
Awarded by DOD ADNI (Department of Defense)
Funding Acknowledgements
Core funding for the AIBL study was provided by the CSIRO Flagship Collaboration Fund and the Science and Industry Endowment Fund (SIEF) in partnership with the CRC for Mental Health, Edith Cowan University (ECU), Mental Health Research institute (MHRI), Alzheimer's Australia (AA), National Ageing Research Institute (NARI), Austin Health, Macquarie University, CogState Ltd, Hollywood Private Hospital, and Sir Charles Gairdner Hospital. The study also received funding from the National Health and Medical Research Council (NHMRC), Dementia Collaborative Research Centres program (DCRC), and McCusker Alzheimer's Research Foundation, and operational infrastructure support from the Government of Victoria. Funding for this study was provided by the NHMRC (Grant Number 1156891). Data collection and sharing for this project was funded by the ADNI (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc; Cogstate; Eisai Inc; Elan Pharmaceuticals, Inc; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc; Fujirebio; GE Healthcare; IXICO Ltd; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co, Inc; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.