E. Klimov, K. Skorobogatykh, O. Rudko, Elena A Naumova, N. Kondratieva, J. Azimova, A. Sergeev, Z. Kokaeva, G. Tabeeva
{"title":"The Influence of Dopamine Beta-Hydroxylase Gene Polymorphism C.-979T>C (Rs1611115) on the Clinical Manifestations of Migraine","authors":"E. Klimov, K. Skorobogatykh, O. Rudko, Elena A Naumova, N. Kondratieva, J. Azimova, A. Sergeev, Z. Kokaeva, G. Tabeeva","doi":"10.15406/JNSK.2018.08.00276","DOIUrl":null,"url":null,"abstract":"Submit Manuscript | http://medcraveonline.com the development of various forms of familial hemiplegic migraine have been identified [2]. A number of others studies have been conducted to better define genetic predisposition to dopamine metabolism disorders. The first study in this field was published in 1997, revealing the DRD2 (D2 dopamine receptor) gene polymorphism, which was found to be significantly more common in patients suffering from migraine with aura [3]. Subsequent studies broadened the scope of searching for potential research targets. All five receptor types were examined, and the next series of experiments failed to confirm changes in the D2DR gene; conflicting data were obtained on the D4 receptor. A study conducted by Todt in 2009 demonstrated that certain alleles of the gene encoding the dopamine transporter SLC6A3 were reliably associated with migraine with aura [4]. This transporter is responsible for reuptake of dopamine from the synaptic cleft, thus acting as a key regulator of dopaminergic activity. Most completed genetic studies have confirmed the role of polymorphism of the gene encoding the enzyme dopamine beta-hydroxylase (DBH), which stimulates the conversion of dopamine to norepinephrine [5-8].","PeriodicalId":106839,"journal":{"name":"Journal of Neurology and Stroke","volume":"45 5 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Neurology and Stroke","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/JNSK.2018.08.00276","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Submit Manuscript | http://medcraveonline.com the development of various forms of familial hemiplegic migraine have been identified [2]. A number of others studies have been conducted to better define genetic predisposition to dopamine metabolism disorders. The first study in this field was published in 1997, revealing the DRD2 (D2 dopamine receptor) gene polymorphism, which was found to be significantly more common in patients suffering from migraine with aura [3]. Subsequent studies broadened the scope of searching for potential research targets. All five receptor types were examined, and the next series of experiments failed to confirm changes in the D2DR gene; conflicting data were obtained on the D4 receptor. A study conducted by Todt in 2009 demonstrated that certain alleles of the gene encoding the dopamine transporter SLC6A3 were reliably associated with migraine with aura [4]. This transporter is responsible for reuptake of dopamine from the synaptic cleft, thus acting as a key regulator of dopaminergic activity. Most completed genetic studies have confirmed the role of polymorphism of the gene encoding the enzyme dopamine beta-hydroxylase (DBH), which stimulates the conversion of dopamine to norepinephrine [5-8].