Paraoxonase 1 gene polymorphisms and dementia in humans

被引：31

作者：

Helbecque, N

Cottel, D

Codron, V

Berr, C

Amouyel, P

机构：

[1] Inst Pasteur, INSERM, U508, Serv Epidemiol & Sante Publ, F-59019 Lille, France

[2] Hop La Colombiere, INSERM, E0331, F-34093 Montpellier, France

[3] Ctr Hosp Reg & Univ Lille, F-59037 Lille, France

来源：

NEUROSCIENCE LETTERS | 2004年 / 358卷 / 01期

关键词：

dementia; polymorphism (genetics); case-control study; esterases;

D O I：

10.1016/j.neulet.2003.12.100

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Several clinical and epidemiological studies suggest that Alzheimer's disease (AD) and vascular dementia share common risk factors. Oxidative stress is one of these well recognized factors. It can result from an excess of free-radical activity and impaired antioxidant defenses. Paraoxonase (PON1), a component of high density lipoproteins, has antioxidative potential and was previously associated with an increased risk of cardiovascular diseases. The impact of two polymorphisms in PON1 (Gln192Arg associated with enzyme activity and T - 107C associated with enzyme concentration) was examined in a case-control study. The two polymorphisms were independent risk factors for nonAD dementia, particularly in APOE-epsilon4 noncarriers. An at-'risk haplotype' could be constructed including the Gln192 and the T - 107 alleles, suggesting that subjects at risk have lower plasma paraoxonase levels and this enzyme is less active. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

引用

页码：41 / 44

页数：4

共 19 条

[1] Inflammation and Alzheimer's disease [J].

Akiyama, H ;

Barger, S ;

Barnum, S ;

Bradt, B ;

Bauer, J ;

Cole, GM ;

Cooper, NR ;

Eikelenboom, P ;

Emmerling, M ;

Fiebich, BL ;

Finch, CE ;

Frautschy, S ;

Griffin, WST ;

Hampel, H ;

Hull, M ;

Landreth, G ;

Lue, LF ;

Mrak, R ;

Mackenzie, IR ;

McGeer, PL ;

O'Banion, MK ;

Pachter, J ;

Pasinetti, G ;

Plata-Salaman, C ;

Rogers, J ;

Rydel, R ;

Shen, Y ;

Streit, W ;

Strohmeyer, R ;

Tooyoma, I ;

Van Muiswinkel, FL ;

Veerhuis, R ;

Walker, D ;

Webster, S ;

Wegrzyniak, B ;

Wenk, G ;

Wyss-Coray, T .

NEUROBIOLOGY OF AGING, 2000, 21 (03) :383-421

[2] The deletion allele of the angiotensin I converting enzyme gene as a genetic susceptibility factor for cognitive impairment [J].

Amouyel, P ;

Richard, F ;

Cottel, D ;

Amant, C ;

Codron, V ;

Helbecque, N .

NEUROSCIENCE LETTERS, 1996, 217 (2-3) :203-205

[3] Pentosidine and Nε-(carboxymethyl)-lysine in Alzheimer's disease and vascular dementia [J].

Bär, KJ ;

Franke, S ;

Wenda, B ;

Müller, S ;

Kientsch-Engel, R ;

Stein, G ;

Sauer, H .

NEUROBIOLOGY OF AGING, 2003, 24 (02) :333-338

[4] Candidate gene association studies in sporadic Alzheimer's disease [J].

Combarros, O ;

Alvarez-Arcaya, A ;

Sánchez-Guerra, M ;

Infante, J ;

Berciano, J .

DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, 2002, 14 (01) :41-54

[5]

DANTOINE M, 2002, ANN NY ACAD SCI, V977, P239

[6]

De La Torre JC, 2002, ANN NY ACAD SCI, V977, P196

[7] Paraoxonase-1 promoter haplotypes and serum paraoxonase: a predominant role for polymorphic position-107, implicating the Sp1 transcription factor [J].

Deakin, S ;

Leviev, I ;

Brulhart-Meynet, MC ;

James, RW .

BIOCHEMICAL JOURNAL, 2003, 372 (372) :643-649

[8] APOE genotype in cerebrovascular disease and vascular dementia [J].

Frank, A ;

Díez-Tejedor, E ;

Bullido, MJ ;

Valdivieso, F ;

Barreiro, P .

JOURNAL OF THE NEUROLOGICAL SCIENCES, 2002, 203 :173-176

[9] Nonsteroidal antiinflammatory drugs and the risk of Alzheimer's disease [J].

in 't Veld, BA ;

Ruitenberg, A ;

Hofman, A ;

Launer, LJ ;

van Duijn, CM ;

Stijnen, T ;

Breteler, MMB ;

Stricker, BHC .

NEW ENGLAND JOURNAL OF MEDICINE, 2001, 345 (21) :1515-1521

[10] Similarities between Alzheimer's disease and vascular dementia [J].

Kalaria, R .

JOURNAL OF THE NEUROLOGICAL SCIENCES, 2002, 203 :29-34

← 1 2 →