Prion protein codon 129 polymorphism and risk of Alzheimer disease

被引：73

作者：

Riemenschneider, M

Klopp, N

Xiang, W

Wagenpfeil, S

Vollmert, C

Müller, U

Förstl, H

Illig, T

Kretzschmar, H

Kurz, A

机构：

[1] Tech Univ Munich, Dept Psychiat & Psychotherapy, Neurochem & Neurogenet Lab, Inst Epidemiol, D-81675 Munich, Germany

[2] Tech Univ Munich, Inst Epidemiol, Dept Med Stat & Epidemiol, D-81675 Munich, Germany

[3] GSF Munich, Res Ctr Environm & Hlth, Genome Anal Ctr, Munich, Germany

[4] Univ Munich, Dept Neuropathol, Munich, Germany

[5] Univ Giessen, Inst Human Genet, D-35390 Giessen, Germany

来源：

NEUROLOGY | 2004年 / 63卷 / 02期

关键词：

D O I：

10.1212/01.WNL.0000130198.72589.69

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The authors investigated the PRNP Met(129)Val polymorphism in 1,393 subjects including 482 patients with Alzheimer disease ( AD) and two independent control groups. In patients, PRNP Met homozygosity conferred increasing risk with decreasing age at onset ( onset: 61 to 70 years, n = 151, p = 0.02, odds ratio [ OR] = 1.72, 95% CI = 1.2 to 2.53; onset: less than or equal to 60 years, n = 138, p = 0.013, OR = 1.92, 95% CI = 1.31 to 2.87), whereas no association was obtained in patients with onset at older than 70 years. The results suggest involvement of the prion protein in the pathogenesis of early-onset AD.

引用

页码：364 / 366

页数：3

共 11 条

[1] Polymorphism of the prion protein is associated with cognitive impairment in the elderly - The EVA study [J].

Berr, C ;

Richard, F ;

Dufouil, C ;

Amant, C ;

Alperovitch, A ;

Amouyel, P .

NEUROLOGY, 1998, 51 (03) :734-737

[2] Polymorphism at codon 129 of the prion protein gene is not associated with sporadic AD [J].

Combarros, O ;

Sánchez-Guerra, M ;

Llorca, J ;

Alvarez-Arcaya, A ;

Berciano, J ;

Peña, N ;

Fernández-Viadero, C .

NEUROLOGY, 2000, 55 (04) :593-595

[3] PRNP Val129 homozygosity increases risk for early-onset Alzheimer's disease [J].

Dermaut, B ;

Croes, EA ;

Rademakers, R ;

Van den Broeck, M ;

Cruts, M ;

Hofman, A ;

van Duijn, CM ;

Van Broeckhoven, C .

ANNALS OF NEUROLOGY, 2003, 53 (03) :409-412

[4]

MCKHANN G, 1984, NEUROLOGY, V34, P939, DOI 10.1212/WNL.34.7.939

[5] Balancing selection at the prion protein gene consistent with prehistoric kurulike epidemics [J].

Mead, S ;

Stumpf, MPH ;

Whitfield, J ;

Beck, JA ;

Poulter, M ;

Campbell, T ;

Uphill, JB ;

Goldstein, D ;

Alpers, M ;

Fisher, EMC ;

Collinge, J .

SCIENCE, 2003, 300 (5619) :640-643

[6] HOMOZYGOUS PRION PROTEIN GENOTYPE PREDISPOSES TO SPORADIC CREUTZFELDT-JAKOB DISEASE [J].

PALMER, MS ;

DRYDEN, AJ ;

HUGHES, JT ;

COLLINGE, J .

NATURE, 1991, 352 (6333) :340-342

[7]

Parchi P, 1999, ANN NEUROL, V46, P224, DOI 10.1002/1531-8249(199908)46:2<224::AID-ANA12>3.0.CO

[8]

2-W

[9] Biochemical and structural studies of the prion protein polymorphism [J].

Petchanikow, C ;

Saborio, GP ;

Anderes, L ;

Frossard, MJ ;

Olmedo, MI ;

Soto, C .

FEBS LETTERS, 2001, 509 (03) :451-456

[10] Case-control study of risk factors of Creutzfeldt-Jakob disease in Europe during 1993-95 [J].

van Duijn, CM ;

Delasnerie-Lauprêtre, N ;

Masullo, C ;

Zerr, I ;

de Silva, R ;

Wientjens, DPWM ;

Brandel, JP ;

Weber, T ;

Bonavita, V ;

Zeidler, M ;

Alpérovitch, A ;

Poser, S ;

Granieri, E ;

Hofman, A ;

Will, RG .

LANCET, 1998, 351 (9109) :1081-1085

← 1 2 →