Apolipoprotein A5 gene C56G variant confers risk for the development of large-vessel associated ischemic stroke

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Abstract

Objectives: Ischemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke. Methods: PCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls. Results: Triglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6%; p <0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smokingand drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95% CI; p <0.05). Conclusion: The data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.

Original languageEnglish
Pages (from-to)649-654
Number of pages6
JournalJournal of Neurology
Volume255
Issue number5
DOIs
Publication statusPublished - máj. 2008

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Apolipoproteins
Stroke
Alleles
Genes
Cholesterol
Serum
Restriction Fragment Length Polymorphisms
Drinking
Habits
Myocardial Ischemia
Diabetes Mellitus
Triglycerides
Logistic Models
Regression Analysis
Hypertension
Polymerase Chain Reaction

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

@article{49bd066e936e4d48bd6a54fa16911f38,
title = "Apolipoprotein A5 gene C56G variant confers risk for the development of large-vessel associated ischemic stroke",
abstract = "Objectives: Ischemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke. Methods: PCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls. Results: Triglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6{\%}; p <0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smokingand drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95{\%} CI; p <0.05). Conclusion: The data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.",
keywords = "APOA5, C56G (S19W), IMT, Ischemic stroke, Susceptibility",
author = "A. Ma{\'a}sz and P. Kisfali and Z. Szolnoki and F. Hadarits and B. Melegh",
year = "2008",
month = "5",
doi = "10.1007/s00415-008-0768-z",
language = "English",
volume = "255",
pages = "649--654",
journal = "Journal of Neurology",
issn = "0340-5354",
publisher = "D. Steinkopff-Verlag",
number = "5",

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TY - JOUR

T1 - Apolipoprotein A5 gene C56G variant confers risk for the development of large-vessel associated ischemic stroke

AU - Maász, A.

AU - Kisfali, P.

AU - Szolnoki, Z.

AU - Hadarits, F.

AU - Melegh, B.

PY - 2008/5

Y1 - 2008/5

N2 - Objectives: Ischemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke. Methods: PCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls. Results: Triglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6%; p <0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smokingand drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95% CI; p <0.05). Conclusion: The data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.

AB - Objectives: Ischemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke. Methods: PCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls. Results: Triglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6%; p <0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smokingand drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95% CI; p <0.05). Conclusion: The data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.

KW - APOA5

KW - C56G (S19W)

KW - IMT

KW - Ischemic stroke

KW - Susceptibility

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U2 - 10.1007/s00415-008-0768-z

DO - 10.1007/s00415-008-0768-z

M3 - Article

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SP - 649

EP - 654

JO - Journal of Neurology

JF - Journal of Neurology

SN - 0340-5354

IS - 5

ER -