Interleukin 1 alpha gene polymorphism as a susceptibility factor in Alzheimer's disease and its influence on the extent of histopathological hallmark lesions of Alzheimer's disease

被引:21
作者
Pirskanen, M
Hiltunen, M
Mannermaa, A
Iivonen, S
Helisalmi, S
Lehtovirta, M
Koivisto, AM
Laakso, M
Soininen, H
Alafuzoff, I
机构
[1] Univ Kuopio, Dept Neurol & Neurosci, FIN-70210 Kuopio, Finland
[2] Kuopio Univ Hosp, Dept Clin Genet, SF-70210 Kuopio, Finland
[3] Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland
[4] Kuopio Univ Hosp, Dept Pathol, SF-70210 Kuopio, Finland
[5] Univ Hosp, Dept Med, Kuopio, Finland
关键词
Alzheimer's disease; interleukin; 1; alpha; polymorphism; senile plaques; neurofibrillary tangles;
D O I
10.1159/000063603
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
We investigated the association of the interleukin la (MA) (-889) C/T polymorphism with Alzheimer's disease (AD) and with the extent of AD histopathological lesions, the senile/neuritic plaques (SPs/NPs) and neurofibrillary tangles. We evaluated 98 neuropathologically confirmed AD patients and 240 controls as well as 146 clinically diagnosed AD patients and 278 controls but found no association of the IL1A C/T polymorphism with AD even after adjustment for the apolipoprotein E (APOE) genotype, gender or age. The extents of AD histopathological lesions were not influenced by the MA genotype except after exclusion of the APOE epsilon4 allele, when a trend towards more SPs/NPs was observed in AD patients with the MA C/C compared to patients with the T/T genotype. These results do not confirm previous studies which have indicated that the lL1A C/T polymorphism is a susceptibility factor for AD. However, the IDA C/C genotype might be associated with the progression of SPs/NPs in AD patients, but the effect is weak and obscured by the APOE epsilon4 allele. Copyright (C) 2002 S. Karger AG, Basel.
引用
收藏
页码:123 / 127
页数:5
相关论文
共 25 条
[1]   CHOLINERGIC AGONISTS AND INTERLEUKIN-1 REGULATE PROCESSING AND SECRETION OF THE ALZHEIMER BETA/A4 AMYLOID PROTEIN-PRECURSOR [J].
BUXBAUM, JD ;
OISHI, M ;
CHEN, HI ;
PINKASKRAMARSKI, R ;
JAFFE, EA ;
GANDY, SE ;
GREENGARD, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) :10075-10078
[2]  
DINARELLO CA, 1991, BLOOD, V77, P1627
[3]   Association of an interleukin 1α polymorphism with Alzheimer's disease [J].
Du, Y ;
Dodel, RC ;
Eastwood, BJ ;
Bales, KR ;
Gao, F ;
Lohmüller, F ;
Müller, U ;
Kurz, A ;
Zimmer, R ;
Evans, RM ;
Hake, A ;
Gasser, T ;
Oertel, WH ;
Griffin, WST ;
Paul, SM ;
Farlow, MR .
NEUROLOGY, 2000, 55 (04) :480-483
[4]   Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease - A meta-analysis [J].
Farrer, LA ;
Cupples, LA ;
Haines, JL ;
Hyman, B ;
Kukull, WA ;
Mayeux, R ;
Myers, RH ;
PericakVance, MA ;
Risch, N ;
vanDuijn, CM .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1997, 278 (16) :1349-1356
[5]   MINI-MENTAL STATE - PRACTICAL METHOD FOR GRADING COGNITIVE STATE OF PATIENTS FOR CLINICIAN [J].
FOLSTEIN, MF ;
FOLSTEIN, SE ;
MCHUGH, PR .
JOURNAL OF PSYCHIATRIC RESEARCH, 1975, 12 (03) :189-198
[6]   INTERLEUKIN-1 REGULATES SYNTHESIS OF AMYLOID BETA-PROTEIN PRECURSOR MESSENGER-RNA IN HUMAN-ENDOTHELIAL CELLS [J].
GOLDGABER, D ;
HARRIS, HW ;
HLA, T ;
MACIAG, T ;
DONNELLY, RJ ;
JACOBSEN, JS ;
VITEK, MP ;
GAJDUSEK, DC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (19) :7606-7610
[7]  
GRIFFIN WST, 1989, P NATL ACAD SCI USA, V86, P7611
[8]  
Grimaldi LME, 2000, ANN NEUROL, V47, P361, DOI 10.1002/1531-8249(200003)47:3<361::AID-ANA12>3.0.CO
[9]  
2-N
[10]  
HIXSON JE, 1990, J LIPID RES, V31, P545