Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10999
Title: Relationship between atrophy and beta-amyloid deposition in Alzheimer disease.
Authors: Chételat, Gaël;Villemagne, Victor L;Bourgeat, Pierrick;Pike, Kerryn E;Jones, Gareth;Ames, David;Ellis, Kathryn A;Szoeke, Cassandra;Martins, Ralph N;O'Keefe, Graeme J;Salvado, Olivier;Masters, Colin L;Rowe, Christopher C
Institutional Author: Australian Imaging Biomarkers and Lifestyle Research Group
Affiliation: Department of Nuclear Medicine and Center for PET, Austin Health, 145 Studley Road, Heidelberg, Victoria 3084, Australia. chetelate@cyceron.fr
Issue Date: 1-Mar-2010
Citation: Annals of Neurology; 67(3): 317-24
Abstract: Elucidating the role of aggregated beta-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 [(11)C]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 beta-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical beta-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional beta-amyloid load was related to local atrophy in the areas of highest beta-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/precuneus areas.There is a strong relationship between beta-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 beta-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.
Internal ID Number: 20373343
URI: http://ahro.austin.org.au/austinjspui/handle/1/10999
DOI: 10.1002/ana.21955
URL: http://www.ncbi.nlm.nih.gov/pubmed/20373343
Type: Journal Article
Subjects: Aged
Aged, 80 and over
Alzheimer Disease.metabolism.pathology.radionuclide imaging
Amyloid beta-Peptides.analysis.metabolism
Atrophy.metabolism.pathology.radionuclide imaging
Benzothiazoles.diagnostic use
Biological Markers.analysis.metabolism
Brain.metabolism.pathology.radionuclide imaging
Cognition Disorders.metabolism.pathology.radionuclide imaging
Disease Progression
Female
Humans
Magnetic Resonance Imaging
Male
Plaque, Amyloid.metabolism.pathology.radionuclide imaging
Positron-Emission Tomography
Predictive Value of Tests
Prognosis
Severity of Illness Index
Appears in Collections:Journal articles

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