Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
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Elizabeta Topic
Abstract
Although controversial, data on the genetic polymorphism of apoprotein E (APOE), methylenetetrahydrofolate (MTHFR) and paraoxonase (PON1) genes implicate their role in the development of cerebrovascular disease. The aim of this study was to assess the association of polymorphism of APOE, MTHFR and PON1 genes in 56 stroke and 36 carotid stenosis patients, and in 124 control subjects by PCR-restriction fragment length polymorphism analysis.
In the stroke group a significantly different MTHFR genotype distribution (p=0.004, odds ratio for T/T of 17.571), but no significant difference in APOE and PON1 allele and genotype distribution compared to the control was found. The carotid stenosis group exhibited a significantly different APOE allele and genotype distribution (p=0.023, odds ratio APOE∊3∊4 of 4.24), but no significant difference in the MTHFR and PON1 allele and genotype distribution from the control group. The preliminary results obtained in this study revealed an association of the MTHFR and APOE gene polymorphism with cerebrovascular disease, suggesting a significant risk for stroke in subjects who are homozygous for the T allele and for carotid stenosis in subjects having APOE∊3∊4 genotype. Additional studies in larger patient groups are needed to confirm these observations.
Copyright © 2001 by Walter de Gruyter GmbH & Co. KG
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Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
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- Neurotrophic Factor Therapy – Prospects and Problems
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