No genetic effect of alpha(1)-antichymotrypsin in Alzheimer disease

被引：90
作者：
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
机构：
[1] MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114
[2] DUKE UNIV,MED CTR,DEPT MED,DIV NEUROL,DURHAM,NC 27710
[3] DUKE UNIV,MED CTR,DUKE COMPREHENS CANC CTR,DURHAM,NC 27710
[4] BOSTON UNIV,MED CTR,DEPT NEUROL,BOSTON,MA
[5] UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024
[6] INDIANA UNIV,MED CTR,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN
来源：
GENOMICS | 1996年 / 33卷 / 01期
关键词：
D O I：
10.1006/geno.1996.0158
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Alzheimer disease (AD) is the most common neurodegenerative disorder for individuals over the age of 40. AD has a complex etiology, and it is likely that multiple genes, acting independently and/or interacting, affect the risk of developing AD. Several genes involved with AD have been described already, but only the APOE gene on chromosome 19q has been shown to affect the risk of the common late onset form of AD. alpha(1)-Antichymotrypsin (AACT) is a major component of the amyloid plaques found in the brains of AD patients, and an allele in its gene has been proposed to increase the risk of developing AD when also associated with the APOE-4 allele. We have examined the role of this AACT polymorphism in a large set of families and sporadic cases, and do not see any effect, either alone or in combination with the APOE-4 allele. (C) 1996 Academic Press, Inc.
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页码：53 / 56
页数：4
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