No effect of the alpha 1-antichymotrypsin A allele in Alzheimer's disease

被引：15

作者：

Didierjean, O

Martinez, M

Campion, D

Hannequin, D

Dubois, B

Martin, C

Puel, M

Anterion, CT

Pasquier, F

Moreau, O

Babron, MC

Penet, C

Agid, Y

ClergetDarpoux, F

Frebourg, T

Brice, A

机构：

[1] HOP LA PITIE SALPETRIERE, INSERM U289, F-75013 PARIS, FRANCE

[2] INSERM U155, F-75016 PARIS, FRANCE

[3] CHU ROUEN, GENET MOL LAB, F-76031 ROUEN, FRANCE

[4] CHU ROUEN, NEUROL CLIN, F-76031 ROUEN, FRANCE

[5] HOP LA PITIE SALPETRIERE, FEDERAT NEUROL, F-75013 PARIS, FRANCE

[6] INSERM U230, F-31059 TOULOUSE, FRANCE

[7] CHU ST ETIENNE, NEUROL CLIN, F-42100 ST ETIENNE, FRANCE

[8] CHU LILLE, NEUROL CLIN, F-59037 LILLE, FRANCE

[9] CHU GRENOBLE, NEUROL CLIN, F-38043 GRENOBLE, FRANCE

来源：

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY | 1997年 / 63卷 / 01期

关键词：

alpha 1-antichymotrypsin (Aact); apolipoprotein E (ApoE); Alzheimer's disease;

D O I：

10.1136/jnnp.63.1.103

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The apolipoprotein E (ApoE)-epsilon 4 allele is associated in a dose dependent manner to an increased risk for Alzheimer's disease. However, the ApoE-epsilon 4 allele effect does not account for all patients with Alzheimer's disease, and the existence of other genetic risk factors has been postulated. Kamboh et al reported an association between Alzheimer's disease and the A allele of alpha 1-antichymotrypsin (Aact) gene, which was not confirmed in a larger series more recently analysed. The ApoE and Aact genotypes were analysed in 314 patients with Alzheimer's disease and 173 healthy controls, confirming the dose dependent effect of the ApoE-epsilon 4 allele. Nevertheless, even using odds ratios adjusted for age and sex, there was no significant effect of the Aact genotype on Alzheimer's disease or on the ApoE-epsilon 4 allele associated risk for Alzheimer's disease.

引用

页码：103 / 105

页数：3

共 15 条

[1] IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE [J].

ABRAHAM, CR ;

SELKOE, DJ ;

POTTER, H .

CELL, 1988, 52 (04) :487-501

[2] GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].

CORDER, EH ;

SAUNDERS, AM ;

STRITTMATTER, WJ ;

SCHMECHEL, DE ;

GASKELL, PC ;

SMALL, GW ;

ROSES, AD ;

HAINES, JL ;

PERICAKVANCE, MA .

SCIENCE, 1993, 261 (5123) :921-923

[3] No genetic effect of alpha(1)-antichymotrypsin in Alzheimer disease [J].

Haines, JL ;

Pritchard, ML ;

Saunders, AM ;

Schildkraut, JM ;

Growdon, JH ;

Gaskell, PC ;

Farrer, LA ;

Auerbach, SA ;

Gusella, JF ;

Locke, PA ;

Rosi, BL ;

Yamaoka, L ;

Small, GW ;

Conneally, PM ;

Roses, AD ;

PericakVance, MA .

GENOMICS, 1996, 33 (01) :53-56

[4]

HAINES JL, 1996, J LIPID RES, V33, P53

[5]

HIXSON JE, 1990, J LIPID RES, V31, P545

[6] APOE-ASTERISK-4-ASSOCIATED ALZHEIMERS-DISEASE RISK IS MODIFIED BY ALPHA-1-ANTICHYMOTRYPSIN POLYMORPHISM [J].

KAMBOH, MI ;

SANGHERA, DK ;

FERRELL, RE ;

DEKOSKY, ST .

NATURE GENETICS, 1995, 10 (04) :486-488

[7] AMYLOID-ASSOCIATED PROTEINS ALPHA(1)-ANTICHYMOTRYPSIN AND APOLIPOPROTEIN-E PROMOTE ASSEMBLY OF ALZHEIMER BETA-PROTEIN INTO FILAMENTS [J].

MA, JY ;

YEE, A ;

BREWER, HB ;

DAS, S ;

POTTER, H .

NATURE, 1994, 372 (6501) :92-94

[8] Segregation analysis of Alzheimer pedigrees: Rare Mendelian dominant mutation(s) explain a minority of early-onset cases [J].

Martinez, M ;

Campion, D ;

Babron, MC ;

Hannequin, D ;

Agid, Y ;

Bellis, M ;

Brice, A ;

Mallet, J ;

Michon, A ;

ThomasAnterion, C ;

ClergetDarpoux, F ;

Dubois, B ;

Goas, Y ;

JaillardSerradt, A ;

Ledoze, F ;

Pasquier, F ;

Puel, M ;

Zimmerman, MA .

AMERICAN JOURNAL OF MEDICAL GENETICS, 1996, 67 (01) :9-12

[9]

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

[10] Evidence for apolipoprotein E epsilon 4 association in early-onset Alzheimer's patients with late-onset relatives [J].

PerezTur, J ;