Journal article
Basal forebrain atrophy correlates with amyloid beta burden in Alzheimer's disease
Georg M Kerbler, Juergen Fripp, Christopher C Rowe, Victor L Villemagne, Olivier Salvado, Stephen Rose, Elizabeth J Coulson
NEUROIMAGE-CLINICAL | ELSEVIER SCI LTD | Published : 2015
Abstract
The brains of patients suffering from Alzheimer's disease (AD) have three classical pathological hallmarks: amyloid-beta (Aβ) plaques, tau tangles, and neurodegeneration, including that of cholinergic neurons of the basal forebrain. However the relationship between Aβ burden and basal forebrain degeneration has not been extensively studied. To investigate this association, basal forebrain volumes were determined from magnetic resonance images of controls, subjects with amnestic mild cognitive impairment (aMCI) and AD patients enrolled in the longitudinal Alzheimer's Disease Neuroimaging Initiative (ADNI) and Australian Imaging, Biomarkers and Lifestyle (AIBL) studies. In the AIBL cohort, the..
View full abstractGrants
Awarded by National Health and Medical Research Council of Australia Career Development Fellowship
Awarded by Alzheimer's Disease Neuroirnaging Initiative (ADNI) (National Institutes of Health)
Awarded by NIH
Awarded by NATIONAL INSTITUTE ON AGING
Funding Acknowledgements
GMK was funded by an ANZ Trustees PhD scholarship for medical research and a University of Queensland International Scholarship. EJC was supported by a National Health and Medical Research Council of Australia Career Development Fellowship (569601). This project was funded by a Mason Foundation grant and Queensland State Government National and International Research Alliance Project grant. The study was partially supported by the Commonwealth Scientific Industrial Research Organisation Preventative Health Flagship Program through the Australian Imaging, Biomarkers, and Lifestyle flagship study of aging, the Austin Hospital Medical Research Foundation, Neurosciences Victoria, and the University of Melbourne. The funding sources had no input into the design of this study, the analysis of data, or writing of the manuscript.r Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroirnaging Initiative (ADNI) (National Institutes of Health grant U01 AG024904). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: Alzheimer's Association; Alzheimer's Drug Discovery Foundation; BioClinica, Inc.; Biogen Idec Inc.; Bristol-Myers Squibb Company; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; GE Healthcare; Innogenetics, N.V.; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research 82 Development, LLC; Johnson & Johnson Pharmaceutical Research and Development LLC; Medpace, Inc.; Merck & Co., Inc.; Meso Scale Diagnostics, LLC; NeuroRx Research; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Synarc Inc.; and Takeda Pharmaceutical Company. The Canadian Institutes of Health Research are providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (http://www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's disease Cooperative Study at the University of California San Diego. ADM data are disseminated by the Laboratory for Neuro Imaging at the University of California Los Angeles. This research was also supported by NIH grants P30 AG010129 and K01 AG030514.