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Titolo:
Positron emission tomography in pallido-ponto-nigral degeneration (PPND) family (frontotemporal dementia with parkinsonism linked to chromosome 17 and point mutation in tau gene)
Autore:
Pal, PK; Wszolek, ZK; Kishore, A; de la Fuente-Fernandez, R; Sossi, V; Uitti, RJ; Dobko, T; Stoessl, AJ;
Indirizzi:
Vancouver Hosp & Hlth Sci Ctr, Ctr Neurodegenerat Disorders, Vancouver, BCV6T 2B5, Canada Vancouver Hosp & Hlth Sci Ctr Vancouver BC Canada V6T 2B5 V6T 2B5, Canada Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA Mayo Clin JacksonvilleFL USA 32224 pt Neurol, Jacksonville, FL 32224 USA
Titolo Testata:
PARKINSONISM & RELATED DISORDERS
fascicolo: 2, volume: 7, anno: 2001,
pagine: 81 - 88
SICI:
1353-8020(200104)7:2<81:PETIPD>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRESSIVE SUPRANUCLEAR PALSY; AUTOSOMAL-DOMINANT PARKINSONISM; CEREBRAL GLUCOSE-UTILIZATION; MULTIPLE SYSTEM ATROPHY; HUNTINGTONS-DISEASE; IDIOPATHIC PARKINSONISM; NIGROSTRIATAL FUNCTION; ALZHEIMERS-DISEASE; PET; METABOLISM;
Keywords:
pallido-ponto-nigral degeneration; Parkinsonism; frontotemporal dementia; positron emission tomography; fluorodopa; dopamine D2 receptors; fluorodeoxyglucose;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Stoessl, AJ Vancouver Hosp & Hlth Sci Ctr, Ctr Neurodegenerat Disorders, Vancouver, BCV6T 2B5, Canada Vancouver Hosp & Hlth Sci Ctr Vancouver BC Canada V6T 2B5 ada
Citazione:
P.K. Pal et al., "Positron emission tomography in pallido-ponto-nigral degeneration (PPND) family (frontotemporal dementia with parkinsonism linked to chromosome 17 and point mutation in tau gene)", PARKINS R D, 7(2), 2001, pp. 81-88

Abstract

Pallido-ponto-nigral degeneration (PPND) is a rapidly progressive disordercharacterized by frontotemporal dementia with parkinsonism unresponsive tolevodopa therapy. In this study, we have further characterized the regional abnormalities of cerebral function using PET with 6-[F-18]fluoro-L-dopa (FD), [C-11] raclopride (RAC), and 2-deoxy-2-fluoro-[F-18]-D-glucose (FDG). FD and RAC scans were performed in 3 patients-2 new patients and a previously reported asymptomatic at-risk individual who became symptomatic 2 years after the first FD scan. Cerebral glucose metabolism was studied by FDG in 2 other patients. In keeping with previous reports, there was a severe reduction of FD uptake, which affected both caudate and putamen to a similar degree in all 3 patients. RAC scans showed normal to elevated striatal D2-receptor binding in all patients. Cerebral glucose metabolism was globally reduced (>2 SD below control mean) in one patient, with maximal involvement offrontal regions, and to a lesser degree in the other patient. Our study showed severe presynaptic dopaminergic dysfunction with intact striatal D2 receptors in PPND patients, implying that the dopa unresponsiveness is probably a result of pathology downstream to the striatum. The pattern of presynaptic dysfunction contrasts with that seen in idiopathic parkinsonism, wherethe putamen is affected more than the caudate nucleus. The pattern of glucose hypometabolism correlates well with the presence of frontotemporal dementia. (C) 2001 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/09/19 alle ore 22:42:31