Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10423
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dc.contributor.authorNg, Steven Y-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorRowe, Christopher C-
dc.date.accessioned2015-05-15T23:52:05Z
dc.date.available2015-05-15T23:52:05Z
dc.date.issued2007-08-01-
dc.identifier.citationArchives of Neurology; 64(8): 1140-4en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10423en
dc.description.abstractA progressive decline in episodic memory affecting activities of daily living is the usual clinical presentation of Alzheimer disease. However, patients presenting with atypical or focal clinical symptoms such as language or visuospatial dysfunction often pose a diagnostic challenge.To explore the presence and topography of beta amyloid (Abeta) as measured by carbon 11-labeled Pittsburgh Compound B ((11)C-PiB) in patients with atypical presentations of dementia.At a tertiary referral center for memory disorders, 15 healthy controls, 10 patients with Alzheimer disease, a patient with primary progressive aphasia (PPA), and a patient with posterior cortical atrophy (PCA) underwent (11)C-PiB positron emission tomographic studies. Retention of (11)C-PiB was compared between different groups using statistical parametric mapping.The topography of cortical (11)C-PiB binding in atypical vs typical Alzheimer disease.Cortical (11)C-PiB binding was higher in the group with Alzheimer disease and in the patients with PPA and PCA than the controls (P < .001). Both patients with atypical dementia had a similar (11)C-PiB binding pattern to Alzheimer disease although (11)C-PiB retention was higher on the left cerebral hemisphere in the patient with PPA (P < .01) and higher in the occipital cortex in the patient with PCA (P < .01).The presence of distinctive focal (11)C-PiB retention patterns was demonstrated in 2 patients with atypical onset of dementia. Pittsburgh Compound B has the potential to facilitate differential diagnosis of dementia and identify patients who could benefit from specific therapeutic strategies aimed at beta amyloid reduction.en
dc.language.isoenen
dc.subject.otherAgeden
dc.subject.otherAlzheimer Disease.metabolism.radionuclide imagingen
dc.subject.otherAmyloid beta-Peptides.metabolismen
dc.subject.otherAniline Compounds.diagnostic useen
dc.subject.otherAphasia, Primary Progressive.metabolism.radionuclide imagingen
dc.subject.otherAtrophyen
dc.subject.otherBrain.radionuclide imagingen
dc.subject.otherCarbon Radioisotopes.diagnostic useen
dc.subject.otherDementia.diagnosis.metabolism.radionuclide imagingen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherParietal Lobe.pathologyen
dc.subject.otherPositron-Emission Tomographyen
dc.subject.otherSyndromeen
dc.subject.otherThiazoles.diagnostic useen
dc.subject.otherTissue Distributionen
dc.titleEvaluating atypical dementia syndromes using positron emission tomography with carbon 11 labeled Pittsburgh Compound B.en
dc.typeJournal Articleen
dc.identifier.journaltitleArchives of neurologyen
dc.identifier.affiliationDepartment of Nuclear Medicine and Centre for Positron Emission Tomography, Austin Health, Melbourne, Australiaen
dc.identifier.doi10.1001/archneur.64.8.1140en
dc.description.pages1140-4en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/17698704en
dc.type.contentTexten
dc.type.austinJournal Articleen
local.name.researcherMasters, Colin L
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptMolecular Imaging and Therapy-
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