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Titolo:
Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease
Autore:
Mega, MS; Chu, T; Mazziotta, JC; Trivedi, KH; Thompson, PM; Shah, A; Cole, G; Frautschy, SA; Toga, AW;
Indirizzi:
Univ Calif Los Angeles, Sch Med, Dept Neurol, Lab Neuro Imaging,Div Brain Mapping, Los Angeles, CA 90095 USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA Univ Calif Los Angeles, Sch Med, Alzheimers Dis Ctr, Los Angeles, CA 90095USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095USA Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90095 USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA
Titolo Testata:
NEUROREPORT
fascicolo: 14, volume: 10, anno: 1999,
pagine: 2911 - 2917
SICI:
0959-4965(19990929)10:14<2911:MBTMFA>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA-PROTEIN; DAMAGE; BRAIN; MRI; CT;
Keywords:
Alzheimer's disease; amyloid protein; brain mapping; PET;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Mega, MS Univ Calif Los Angeles, Sch Med, Dept Neurol, Lab Neuro Imaging,Div Brain Mapping, 710 Westwood Plaza,Rm 4-238 Reed, Los Angeles, CA 90095 USA Univ Calif Los Angeles 710 Westwood Plaza,Rm 4-238 Reed Los Angeles CA USA 90095
Citazione:
M.S. Mega et al., "Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease", NEUROREPORT, 10(14), 1999, pp. 2911-2917

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 [F-18]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 regionsof the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have otherfactors that contribute to metabolic deficits. (C) 1999 Lippincott Williams & Wilkins.

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Documento generato il 14/07/20 alle ore 19:47:47