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Relationship between atrophy and β-amyloid deposition in Alzheimer disease
Article first published online: 23 DEC 2009
Copyright © 2010 American Neurological Association
Annals of Neurology
Volume 67, Issue 3, pages 317–324, March 2010
How to Cite
Chételat, G., Villemagne, V. L., Bourgeat, P., Pike, K. E., Jones, G., Ames, D., Ellis, K. A., Szoeke, C., Martins, R. N., O'Keefe, G. J., Salvado, O., Masters, C. L. and Rowe, C. C. (2010), Relationship between atrophy and β-amyloid deposition in Alzheimer disease. Ann Neurol., 67: 317–324. doi: 10.1002/ana.21955
- Issue published online: 29 MAR 2010
- Article first published online: 23 DEC 2009
- Accepted manuscript online: 23 DEC 2009 12:00AM EST
- Manuscript Accepted: 14 DEC 2009
- Manuscript Revised: 7 DEC 2009
- Manuscript Received: 27 OCT 2009
- Commonwealth Scientific Industrial Research Organization (CSIRO)
- Australian Imaging, Biomarkers and Lifestyle (AIBL) flagship study of aging
- Austin Hospital Medical Research Foundation
- Neurosciences Victoria
- University of Melbourne
Elucidating the role of aggregated β-amyloid in relation to gray matter atrophy is crucial to the understanding of the pathological mechanisms of Alzheimer disease and for the development of therapeutic trials. The present study aims to assess this relationship.
Brain magnetic resonance imaging and [11C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group.
Global and regional atrophy were strongly related to β-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical β-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional β-amyloid load was related to local atrophy in the areas of highest β-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/precuneus areas.
There is a strong relationship between β-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated β-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss. ANN NEUROL 2010;67:317–324