Publications
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Mapping biochemistry to metabolism: FDG-PET and amyloid burden in
Alzheimer's disease
Source: Neuroreport 1999 Sep;10(14):2911-2917.
Author: Mega MS, Chu T, Mazziotta JC, Trivedi KH, Thompson PM, Shah A, Cole G, Frautschy SA, Toga AW.
PubMed ID: 10549796
Abstract:
We evaluated the relationship between amyloid-beta protein (A beta) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and A beta deposition. Findings support A beta as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.
Source: Neuroreport 1999 Sep;10(14):2911-2917.
Author: Mega MS, Chu T, Mazziotta JC, Trivedi KH, Thompson PM, Shah A, Cole G, Frautschy SA, Toga AW.
PubMed ID: 10549796
Abstract:
We evaluated the relationship between amyloid-beta protein (A beta) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and A beta deposition. Findings support A beta as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.