Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10380
Title: Imaging beta-amyloid burden in aging and dementia.
Authors: Rowe, Christopher C;Ng, S;Ackermann, Uwe;Gong, Sylvia J;Pike, Kerryn E;Savage, Greg;Cowie, T F;Dickinson, K L;Maruff, Paul;Darby, David G;Smith, C;Woodward, Michael M;Merory, J;Tochon-Danguy, Henri;O'Keefe, Graeme J;Klunk, W E;Mathis, C A;Price, J C;Masters, Colin L;Villemagne, Victor L
Affiliation: christopher.rowe@austin.org.au
Department of Nuclear Medicine, Centre for PET, Austin Health, Heidelberg, Victoria, Australia
Issue Date: 15-May-2007
Citation: Neurology; 68(20): 1718-25
Abstract: To compare brain beta-amyloid (Abeta) burden measured with [(11)C]Pittsburgh Compound B (PIB) PET in normal aging, Alzheimer disease (AD), and other dementias.Thirty-three subjects with dementia (17 AD, 10 dementia with Lewy bodies [DLB], 6 frontotemporal dementia [FTD]), 9 subjects with mild cognitive impairment (MCI), and 27 age-matched healthy control subjects (HCs) were studied. Abeta burden was quantified using PIB distribution volume ratio.Cortical PIB binding was markedly elevated in every AD subject regardless of disease severity, generally lower and more variable in DLB, and absent in FTD, whereas subjects with MCI presented either an "AD-like" (60%) or normal pattern. Binding was greatest in the precuneus/posterior cingulate, frontal cortex, and caudate nuclei, followed by lateral temporal and parietal cortex. Six HCs (22%) showed cortical uptake despite normal neuropsychological scores. PIB binding did not correlate with dementia severity in AD or DLB but was higher in subjects with an APOE-epsilon4 allele. In DLB, binding correlated inversely with the interval from onset of cognitive impairment to diagnosis.Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. Noninvasive longitudinal studies to better understand the role of amyloid deposition in the course of neurodegeneration and to determine if Abeta deposition in nondemented subjects is preclinical AD are now feasible. Our findings also suggest that Abeta may influence the development of dementia with Lewy bodies, and therefore strategies to reduce Abeta may benefit this condition.
Internal ID Number: 17502554
URI: http://ahro.austin.org.au/austinjspui/handle/1/10380
DOI: 10.1212/01.wnl.0000261919.22630.ea
URL: http://www.ncbi.nlm.nih.gov/pubmed/17502554
Type: Journal Article
Subjects: Aged
Aged, 80 and over
Aging.metabolism.pathology
Alzheimer Disease.metabolism.pathology.radionuclide imaging
Amyloid beta-Peptides.analysis
Aniline Compounds.diagnostic use
Apolipoproteins E.genetics
Brain Chemistry
Carbon Radioisotopes.diagnostic use
Cognition Disorders.metabolism.pathology.radionuclide imaging
Dementia.metabolism.pathology.radionuclide imaging
Female
Gyrus Cinguli.chemistry.radionuclide imaging
Humans
Lewy Body Disease.metabolism.pathology.radionuclide imaging
Magnetic Resonance Imaging
Male
Middle Aged
Neocortex.chemistry.radionuclide imaging
Radiopharmaceuticals.diagnostic use
Thiazoles.diagnostic use
Appears in Collections:Journal articles

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