E-ISSN 2636-865X
Research Article
ACE I/D and MTHFR C677T Gene Polymorphisms and Matrix Metalloproteinase-9 Gene Expression in Migraine Patients with and without Aura and Correlation with Cranial Magnetic Resonance Imaging Findings: A Case-Control Study
1 Izmir University Medical Faculty Medicalpark Hospital, Department of Neurology, Izmir, Turkey  
2 Ege University Medical Faculty Hospital, Department of Neurology, Izmir, Turkey  
3 Ege University Medical Faculty, Department of Medical Genetic, Izmir, Turkey  
4 Ege University Medical Faculty, Department of Radiodiagnostic, Neuroradiology Field, Izmir, Turkey  
5 Ege University Medical Faculty, Department of Biostatistics and Medical Informatics, Izmir, Turkey  
Neurol Sci Neurophysiol 2015; 32: 348-360

Key Words: Migraine, ACE I/D, MTHFR C677T, MMP-9, cranial MRI
Abstract

Aim: To investigate methylenetetrahydrofolate reductase (MTHFR) C677T and angiotensin converting enzyme (ACE) I/D gene polymorphisms and matrix metalloproteinase 9 (MMP-9) gene expression in migraine patients and correlation with cranial magnetic resonance imaging (MRI) findings.

 

Methods: Migraine patients with (n=50) and without aura (n=50) and age- and gender-matched healthy individuals (n=100) were included. MTHFR C677T and ACE I/D gene polymorphisms and MMP-9 gene expression were explored in the blood samples. Volumes of hyperintense lesions detected on MRI were calculated.

 

Results: No significant difference was determined among the migraine patients with and without aura and controls regarding MTHFR C677T and ACE I/D genotype distribution and MMP-9 gene expression. Comparing all migraine patients with controls, the rate of ACE I/D genotype was higher in the patients, whereas DD genotype was higher in the controls. The number and volume of MRI lesions were significantly higher in the migraine patients with aura as compared to the controls. The number of lesions was higher in ACE DD genotype group than in the ID genotype group.

 

Conclusions: Migraine was a risk factor for silent hyperintense cerebral lesions; however, the role of MTHFR C677T and ACE I/D gene polymorphism and MMP-9 gene expression in migraine pathophysiology remained unresolved.

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