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Titolo:
Parkinson's disease, CYP2D6 polymorphism, and age
Autore:
Payami, H; Lee, N; Zareparsi, S; McNeal, MG; Camicioli, R; Bird, TD; Sexton, G; Gancher, S; Kaye, J; Calhoun, D; Swanson, PD; Nutt, J;
Indirizzi:
Univ Washington, Dept Neurol, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 , Dept Neurol, Seattle, WA 98195 USA Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA USA Vet Affairs Puget Sound Hlth Care Syst Seattle WA USA t, Seattle, WA USA Kaiser Permanente, Portland, OR USA Kaiser Permanente Portland OR USAKaiser Permanente, Portland, OR USA Oregon Hlth Sci Univ, Dept Publ Hlth & Preventat Med, Portland, OR 97201 USA Oregon Hlth Sci Univ Portland OR USA 97201 at Med, Portland, OR 97201 USA Oregon Hlth Sci Univ, Dept Mol & Med Genet, Portland, OR 97201 USA Oregon Hlth Sci Univ Portland OR USA 97201 Genet, Portland, OR 97201 USA Oregon Hlth Sci Univ, Dept Neurol, Portland, OR 97201 USA Oregon Hlth Sci Univ Portland OR USA 97201 Neurol, Portland, OR 97201 USA
Titolo Testata:
NEUROLOGY
fascicolo: 10, volume: 56, anno: 2001,
pagine: 1363 - 1370
SICI:
0028-3878(20010522)56:10<1363:PDCPAA>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDROXYLASE GENE POLYMORPHISM; ALPHA-SYNUCLEIN GENE; APOLIPOPROTEIN-E; ALLELIC FREQUENCIES; ALZHEIMERS-DISEASE; HUMAN LONGEVITY; EARLY-ONSET; E GENOTYPE; 2D6 GENE; DEBRISOQUINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Payami, H Oregon Hlth Sci Univ, Dept Neurol, 3181 SW Sam Jackson Pk Rd,CR131, Portland, OR 97201 USA Oregon Hlth Sci Univ 3181 SW Sam Jackson Pk Rd,CR131 Portland OR USA 97201
Citazione:
H. Payami et al., "Parkinson's disease, CYP2D6 polymorphism, and age", NEUROLOGY, 56(10), 2001, pp. 1363-1370

Abstract

Objective: PD may be caused by genetic susceptibility to neurotoxins. CYP2D6 is a candidate gene for PD because it regulates drug and toxin metabolism, but association studies have been inconsistent. The aim of this study was to test if the CYP2D6*4 allele (poor metabolizer phenotype) is associatedwith earlier age at onset. Methods: Five hundred seventy-six patients withPD and 247 subjects without PD were studied using standard diagnostic, genotyping, and statistical techniques. Results: Surprisingly, mean onset age was significantly later in *4-positive patients. Frequency of *4 was significantly higher in late-onset FD than early-onset PD. When early- and late-onset PD were analyzed separately, *4 had no effect on onset age; hence, theassociation with delayed onset was likely an artifact of an elevated *4 frequency in late-onset PD. Contrary to a common assumption that CYP2D6 frequencies do not change with age, *4 frequency rose significantly with advancing age, both in patients with PD (from 0.16 at mean age of 56.5 years to 0.21 at mean age of 72) and subjects without PD (from 0.09 at mean age of 45.5 years to 0.21 act mean age of 72). *4 Frequencies in patients with early-and late-onset PD, although different from each other, were in agreement with similarly aged subjects without PD, suggesting the elevated *4 frequency in late-onset PD was likely an age effect, unrelated to PD. Conclusion: The CYP2D6*4 allele is not associated with earlier PD onset. *4 May be associated with survival. Inconsistent results from allelic association studies may have been due to an unrecognized age effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/07/20 alle ore 08:40:59