ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER'S DISEASE
中国医学科学杂志(英文版)2004年0卷第2期 页码:93-96
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ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER'S DISEASE
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Author bio:
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Supported by a grant from the Heilongjiang Provincial Natural Science Foundation (D01-21) and partly by the National Postdoctoral Research Foundation (LRB 00071).
DOI:
中图分类号:R749.1
纸质出版日期:2004
Accepted:
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ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER'S DISEASE[J]. 中国医学科学杂志(英文版), 2004,0(2):93-96.
ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER’S DISEASE[J]. Chinese medical sciences journal, 2004, 0(2): 93-96.
ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER'S DISEASE[J]. 中国医学科学杂志(英文版), 2004,0(2):93-96.DOI:
ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER’S DISEASE[J]. Chinese medical sciences journal, 2004, 0(2): 93-96.DOI:
ANALYSIS OF INTERLEUKIN-1 RECEPTOR ANTAGONIST GENE POLYMORPHISM IN CHINESE PATIENTS WITH ALZHEIMER'S DISEASE
摘要
Abstract
Objective To identify an interaction between the interleukin-1 receptor antagonist gene polymorphism and risk of Al-zheimer’s disease. Methods The study included 117 healthy controls
85 patients with Alzheimer’s disease in a Northeastern Chinese popu-lation of Han nationality. Genotypes were determined by a polymerase chain reaction amplification of the intron 2 fragment
harbouring a variable number of short tandem nucleotide sequences. Amplification products were separated on a 2% agarose gel. Results The allele 2 frequency was 27% in healthy controls
and 21% in patients with Alzheimer’s disease. Thus for all-ele 2 as well as for all other alleles
genotypes
or carriage rates
no significant differences compared with controls. Conclusions No association of interleukin-1 receptor antagonist gene polymorphism with Alzheimer’s disease was iden-tified in this population. It is also possible that the increased risk and disease modifying effects are caused by linkage disequ-ilibrium with other genomic variants in other nearby genes.