Molecular factors in migraine
Metrics: PDF 1845 views | HTML 2518 views | ?
Marta Kowalska1, Michał Prendecki1, Wojciech Kozubski2, Margarita Lianeri1 and Jolanta Dorszewska1
1 Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
2 Chair and Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
Jolanta Dorszewska, email:
Keywords: gene polymorphisms, biochemical factors, migraine
Received: October 07, 2015 Accepted: May 05, 2016 Published: May 14, 2016
Migraine is a common neurological disorder that affects 11% of adults worldwide. This disease most likely has a neurovascular origin. Migraine with aura (MA) and more common form - migraine without aura (MO) – are the two main clinical subtypes of disease. The exact pathomechanism of migraine is still unknown, but it is thought that both genetic and environmental factors are involved in this pathological process. The first genetic studies of migraine were focused on the rare subtype of MA: familial hemiplegic migraine (FHM). The genes analysed in familial and sporadic migraine are: MTHFR, KCNK18, HCRTR1, SLC6A4, STX1A, GRIA1 and GRIA3. It is possible that migraine is a multifactorial disease with polygenic influence.
Recent studies have shown that the pathomechanisms of migraine involves both factors responsible for immune response and oxidative stress such as: cytokines, tyrosine metabolism, homocysteine; and factors associated with pain transmission and emotions e.g.: serotonin, hypocretin-1, calcitonin gene-related peptide, glutamate. The correlations between genetic variants of the HCRTR1 gene, the polymorphism 5-HTTLPR and hypocretin-1, and serotonin were observed. It is known that serotonin inhibits the activity of hypocretin neurons and may affect the appearance of the aura during migraine attack.
The understanding of the molecular mechanisms of migraine, including genotype-phenotype correlations, may contribute to finding markers important for the diagnosis and treatment of this disease.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.