Monoamine oxidases A and B gene polymorphisms in migraine patients

Filić, Vedrana; Vladić, Anton; Štefulj, Jasminka; Čičin‐Šain, Lipa; Balija, Melita; Sučić, Zvonimir; Jernej, Branimir

doi:10.1016/j.jns.2004.11.045

Cited by 34 publications

(21 citation statements)

References 32 publications

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“…We assume that this polymorphism is inherited together with another one influencing thus the protein structure or any other transcription regulation and the synthesized protein 89 . As opposed to these findings, other authors did not show any association between the enzyme activity and the genotype 90 . The results point to different tissue-specific control mechanisms of the MAO-B activity in the platelets and in the brain.…”

Section: Polymorphic Gene Variant For Mao-b and Alcohol Addictioncontrasting

confidence: 83%

Neurobiological Bases of Alcohol Addiction

Matošić¹,

Marušić²,

Vidrih³

et al. 2016

ACC

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SUMMARY -Alcohol addiction is a heterogeneous psychiatric disorder according to both phenotype and etiology. Difference in phenotype characteristics manifests in the manner the addiction arises, history of the alcoholic and history of drinking, comorbid disorders, and the phenomenon of abstinence difficulties. Concerning the etiology of alcoholism, the disease itself is considered to be a consequence of an interactive influence of the environment and genetic factors. Numerous researches conducted in the last decades discovered many aspects of the biochemical, cell and molecular bases of alcohol addiction, leading to a conclusion that alcoholism is, like many other addictions, a brain disease. By recognizing alcoholism as a disease which basically implies changes of the neurobiological mechanisms, as well as a clear genetic basis, it was supposed that the disease, having its basis solely in the symptomatology, is essentially heterogeneous. By trying to solve the problem of a clinically heterogeneous nature of the disease during the last fifty years, various sub-classifications of such patients have been suggested. According to Cloninger, subtypes of alcoholism differ also according to changes in the brain neurotransmission systems, i.e. it is supposed that patients suffering from alcoholism type 1 have a more pronounced dopaminergic transmission deficit, while dopaminergic transmission is not disturbed significantly in patients diagnosed with alcoholism type 2, who, however, have a significant lack of serotonergic transmission. In such a way, Cloninger actually presented the basis of the so-called neurobiological alcoholism model. Since he has connected differences in neurotransmission with differences in personality characteristics, this model is also known as the psychobiological model of alcoholism. The characteristic of alcoholism type 1 is avoiding damage (Harm Avoidance, HA) decreased dopamine transmission and increased serotonin transmission, while the significant characteristic of alcoholism type 2 is seeking for excitement (Novelty Seeking, NS), unchanged dopamine transmission and decreased serotonin transmission. These neurochemical differences among alcoholism subtypes represent the basis for a different therapy approach. Intake of alcohol changes different gene expression in the human brain. The inheritance model of alcoholism is not fully explained, however, it is considered that the disease is connected to a larger gene number included in neurotransmission, cell mechanisms and general metabolic function, with a simultaneous influence of the environment. The contribution of genetic factors is stronger in certain types of alcoholism and thus we have been confronted in the last years of alcoholism research with studies researching the connections of some alcoholism subtypes with the polymorphism phenomenon in the genes coding the synaptic proteins included in the alcoholism etiology. The primary role of monoamine oxidase (MAO) in the brain is catalysis of deamination of the oxidative neurotransmitter a...

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Section: Polymorphic Gene Variant For Mao-b and Alcohol Addictioncontrasting

confidence: 83%

Neurobiological Bases of Alcohol Addiction

Matošić¹,

Marušić²,

Vidrih³

et al. 2016

ACC

View full text Add to dashboard Cite

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“…In a 2005 study investigating the polymorphism of MAO-A and -B genes, the authors identified a tendency towards an association of MAO-A with migraine without aura in male subjects while there was no association of MAO-B polymorphism or MAO-B activity with migraine (Filic et al, 2005). These data suggest a re-evaluation of RIMAs for their clinical effect in the prevention of migraine episodes.…”

Section: Migraine and Tension Type Headachementioning

confidence: 99%

Monoamine Oxidase Inhibitors—Revisiting a Therapeutic Principle

Entzeroth¹,

Ratty²

2017

OJD

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Over more than 60 years, monoamine oxidase (MAO) inhibitors are available for therapy of central nervous diseases. Although they have shown to be efficacious specifically in the treatment of major depressive disorders and treatment-resistant depression, they became less a therapeutic choice for the physicians mostly due to severe side effects, such as liver failure and hypertensive crisis associated specifically with the first generation of inhibitors. Nevertheless, this class of drugs is still being used for treatment specifically as more selective and reversible inhibitors became available and will provide clinicians with additional treatment options. The current review revisits monoamine oxidase inhibitors and their potential in the treatment of human diseases, such as anxiety, depression, mood and personality disorders, and pain and introduces current ideas and developments.

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“…Their study provided data for an enhanced vulnerability to suicide in depressed males with major depressive disorder, associated with the MAOA 4R allele [24]. In a study by Filic V et al, no association was detected in migraine patients with and without aura [22]. Another study revealed that plasma 5-HT levels in migraine patients without aura are lower when compared to controls, based on the higher G allele and G/G genotype of T941G polymorphisms of MAOA in migraine patients [25].…”

Section: Discussionmentioning

confidence: 95%

“…Related studies have shown that MAOA gene mutations could be associated with borderline mental retardation and abnormal behavior, including increased impulsive behavior [21]. The association between MAOA promoter region polymorphism and migraine was also investigated, but no relation was found [22]. Kelada et al suggested that the G allele of MAOB had approximately two times the increased risk for PD [23].…”

Section: Discussionmentioning

confidence: 99%

Association Analysis of the Functional MAOA Gene Promoter and MAOB Gene Intron 13 Polymorphisms in Tension Type Headache Patients

Edgnülü¹,

Özge²,

Erdal³

et al. 2014

Adv Clin Exp Med

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Background. Monoamine oxidase (MAO) enzymes play an important role in the etiology of many neurological diseases. Tension type headache (TTH) treatments contain inhibitors for selective re-uptake of serotonin and monoamine oxidase inhibitors. MAO (EC 1.4.3.4) has two isoenzymes known as MAOA and MAOB. A promoter polymorphism of a variable number of tandem repeats (VNTR) in the MAOA gene seems to affect MAOA transcriptional activity in vitro. Also, G/A polymorphism in intron 13 (rs1799836) of the MAOB gene have been previously found to be associated with the variability of MAOB enzyme activity. Objectives. The aim of our study was to investigate a possible association of monoamine oxidase (MAOA and MAOB) gene polymorphisms in tension type headache. Material and Methods. MAO gene polymorphisms were examined in a group of 120 TTH patients and in another 168 unrelated healthy volunteers (control group). MAOA promoter and MAOB intron 13 polymorphisms were genotyped using PCR-based methods.Results. An overall comparison between the genotype of MAOA and MAOB genes and allele frequencies of the patients and the control group did not reveal any statistically significant difference between the patients and the control group (p = 0.162). Conclusions. Factors like estrogen dosage, the limited number of male patients and other genes' neurotransmitters involved in the etiology of TTH could be responsible for our non-significant results (Adv Clin Exp Med 2014, 23, 6, 901-906).

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Monoamine oxidases A and B gene polymorphisms in migraine patients

Cited by 34 publications

References 32 publications

Neurobiological Bases of Alcohol Addiction

Neurobiological Bases of Alcohol Addiction

Monoamine Oxidase Inhibitors—Revisiting a Therapeutic Principle

Association Analysis of the Functional MAOA Gene Promoter and MAOB Gene Intron 13 Polymorphisms in Tension Type Headache Patients

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