Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease.
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.
Mega
M S
MS
Department of Neurology, UCLA School of Medicine, Los Angeles, CA 90095-1769, USA.
Chu
T
T
Mazziotta
J C
JC
Trivedi
K H
KH
Thompson
P M
PM
Shah
A
A
Cole
G
G
Frautschy
S A
SA
Toga
A W
AW
D000368:Aged; D000369:Aged, 80 and over; D000465:Algorithms; D000544:Alzheimer Disease / Q000000981:diagnostic imaging* / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D001822:Body Burden; D001923:Brain Chemistry / Q000502:physiology; D001931:Brain Mapping; D019788:Fluorodeoxyglucose F18; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D019275:Radiopharmaceuticals; D014055:Tomography, Emission-Computed
D016229:Amyloid beta-Peptides; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18