Taq1A Polymorphism Research Articles

Cumulative Genetic Scores Interact with Maternal and Paternal Parenting in Predicting Parent-Adolescent Cohesion and Conflict.

Previous research concerning the interplay between genetics and parenting in the development of the parent-child relationship during adolescence has been extremely scarce, predominantly adopting single-gene designs. This limited body of work has largely overlooked the distinct effects of maternal and paternal roles, as well as potential gender differences. Additionally, existing gene-by-environment (G × E) studies have mainly concentrated on adverse environmental factors and associated negative outcomes, somewhat neglecting positive environments and outcomes. The present study examined the interactions of cumulative genetic scores (CGS, dopamine receptor D2 TaqIA and oxytocin receptor gene rs53576 polymorphisms) with both positive and negative parenting on parent-adolescent cohesion and conflict. Furthermore, this study aimed to ascertain with which gene-environment model the potential G × E interactions would align. A total of 745 Chinese Han adolescents (Mage = 13.36 ± 0.96 years; 46.8% girls) from grades 7 to 9 participated in this study. Results revealed a significant effect of CGS and negative maternal parenting on mother-adolescent conflict among males, consistent with the weak differential susceptibility model. As CGS increased, the effects of negative maternal parenting on mother-son conflict were magnified. These findings have implications for the timing and focus of interventions aimed at improving parent-adolescent relationships.

Association between dopamine receptor D2 Taq IA gene polymorphism (rs1800497) and personality traits.

This study aimed to find a potential association between the DRD2 Taq1A gene polymorphism (rs1800497 C32806T) and personality traits. In all, 249 youths were recruited for this study. The Short-form Revised Eysenck Personality Questionnaire was administered to assess personality traits. The participants were genotyped for the DRD2 Taq1A polymorphism using the polymerase chain reaction-restriction fragment length polymorphism method. Statistical analysis was carried out to find a possible association between the genotypes and aspects of personality traits assessed. The frequencies of the A1 and A2 alleles in our sampled population were 215 (43.2%) and 283 (56.8%), while the frequencies of A1A1, A1A2, and A2A2 were 67 (26.9%), 81 (32.5%), and 101 (40.6%), respectively. The study population was not in Hardy-Weinberg equilibrium (χ2 = 17.64, p < 0.001). The A2 allele was significantly associated with extraversion. Although this allele was also associated with neuroticism, psychoticism, and lie, the association was not significant. The A2 allele of the DRD2 Taq1A polymorphism was found to be more associated with extraversion, as measured by the Short-form Revised Eysenck Personality Questionnaire.

Blocking D2/D3 dopamine receptors in male participants increases volatility of beliefs when learning to trust others

The ability to learn about other people is crucial for human social functioning. Dopamine has been proposed to regulate the precision of beliefs, but direct behavioural evidence of this is lacking. In this study, we investigate how a high dose of the D2/D3 dopamine receptor antagonist sulpiride impacts learning about other people’s prosocial attitudes in a repeated Trust game. Using a Bayesian model of belief updating, we show that in a sample of 76 male participants sulpiride increases the volatility of beliefs, which leads to higher precision weights on prediction errors. This effect is driven by participants with genetically conferred higher dopamine availability (Taq1a polymorphism) and remains even after controlling for working memory performance. Higher precision weights are reflected in higher reciprocal behaviour in the repeated Trust game but not in single-round Trust games. Our data provide evidence that the D2 receptors are pivotal in regulating prediction error-driven belief updating in a social context.

DRD2 TaqIA polymorphism-related functional connectivity between anterior insula and dorsolateral prefrontal cortex predicts the retention time in heroin-dependent individuals under methadone maintenance treatment.

Dopamine receptor D2 (DRD2) TaqIA polymorphism has an influence on addiction treatment response and prognosis by mediating brain dopaminergic system efficacy. Insula is crucial for conscious urges to take drugs and maintain drug use. However, it remains unclear about the contribution of DRD2 TaqIA polymorphism to the regulation of insular on addiction behavioral and its relation with the therapeutic effect of methadone maintenance treatment (MMT). 57 male former heroin dependents receiving stable MMT and 49 matched male healthy controls (HC) were enrolled. Salivary genotyping for DRD2 TaqA1 and A2 alleles, brain resting-state functional MRI scan and a 24-month follow-up for collecting illegal-drug-use information was conducted and followed by clustering of functional connectivity (FC) patterns of HC insula, insula subregion parcellation of MMT patients, comparing the whole brain FC maps between the A1 carriers and non-carriers and analyzing the correlation between the genotype-related FC of insula sub-regions with the retention time in MMT patients by Cox regression. Two insula subregions were identified: the anterior insula (AI) and the posterior insula (PI) subregion. The A1 carriers had a reduced FC between the left AI and the right dorsolateral prefrontal cortex (dlPFC) relative to no carriers. And this reduced FC was a poor prognostic factor for the retention time in MMT patients. DRD2 TaqIA polymorphism affects the retention time in heroin-dependent individuals under MMT by mediating the functional connectivity strength between left AI and right dlPFC, and the two brain regions are promising therapeutic targets for individualized treatment.

Taq1A polymorphism in patients with bipolar disorder: A candidate gene study based on the dopamine hypothesis

Taq1A polymorphism in patients with bipolar disorder: A candidate gene study based on the dopamine hypothesis

Analysis of Factors Associated with Outcomes of Bariatric Surgery: rs1800497 ANKK1, rs1799732 DRD2 Genetic Polymorphisms, Eating Behavior, Hedonic Hunger, and Depressive Symptoms

IntroductionA therapeutic approach to severe obesity is bariatric surgery (BS), which is considered an effective intervention for ameliorating comorbidities such as T2DM, hypertension, dyslipidemia, and cardiovascular diseases. Some polymorphisms are considered markers for addictive disorders and hedonic hunger. We analyzed factors associated with the outcomes of BS, including rs1800497 ANKK1 and rs1799732 DRD2 polymorphisms, eating behavior, hedonic hunger, and depressive symptoms. MethodsWe retrospectively selected 101 patients who underwent BS and agreed to participate. The previous conditions to BS, such as body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), and comorbidities, were registered; the scholarship value was evaluated as the total number of years of scholarly education. To evaluate the post-surgery conditions of the participants, we took blood samples, anthropometric measures, and 3 questionnaires to evaluate eating behavior (TFEQ-R18), hedonic hunger (PFS), and depressive symptoms (PHQ-9). The ANKK1 rs1800497 and rs1799732 DRD2 polymorphisms were genotyped. ResultsThe median total weight loss (TWL) was 34.7 kg, with a BMI of 33.8 kg/m2, 6 (4–8) years after BS. The TWL was positively associated with the TFEQ-R18 score (p = 0.006) and negatively associated with triglycerides (p = 0.011). rs1800497 ANKK1 was associated with TFEQ-R18 (OR = 1.13 (1.02–1.25), p = 0.009). We also found a negative correlation of pre-surgery BMI with scholarship (r = − 0.27, p < 0.05). ConclusionThe patients showed an improvement in metabolic and anthropometric parameters post-surgery. Interestingly, the ANKK1 Taq1A polymorphism was associated with eating behavior and scholarship with pre-surgery BMI, which may be considered predictors of BS outcomes.

Evaluation of the Relationship Between Dopamine Receptor D2 Gene TaqIA1 Polymorphism and Alcohol Dependence Risk.

Several studies are published, that investigated dopamine receptor 2 (DRD2) gene TaqIA polymorphism as a risk factor for alcohol dependence (AD) with positive and negative associations. To derive a more precise estimation of the relationship, a meta-analysis of case-control studies that examined the association between DRD2 gene Taq1A polymorphism and alcohol dependence was performed. Eligible articles were identified through a search of databases including PubMed, Science Direct, Springer link, and Google Scholar. The association between the DRD2 TaqIA polymorphism and AD susceptibility was conducted using odds ratios (ORs) and 95% confidence intervals (95% CIs) as association measures. A total of 69 studies with 9125 cases and 9123 healthy controls were included in the current meta-analysis. Results of the present analysis showed significant association between DRD2 TaqIA polymorphism and AD risk using five genetic modes (allele contrast model-OR 1.22, 95% CI 1.13-1.32, p < 0.0001; homozygote model-OR 1.35, 95%CI 1.18-1.55; p ≤ 0.0001; dominant model-OR 1.29; 95% CI 1.20-1.39; p < 0.0001; recessive model-OR 1.21; 95% CI 1.08-1.36; p = 0.0006). There was no significant association found in subgroup analysis, TaqIA polymorphism was not significantly associated with AD risk in the Asian population under all genetic models, but in the Caucasian population, TaqIA polymorphism was significantly associated with AD risk. Overall, results support the hypothesis that DRD2 Taq1A polymorphism plays a role in alcohol dependence.

The Addiction-Susceptibility TaqIA/Ankk1 Controls Reward and Metabolism Through D2 Receptor-Expressing Neurons

BackgroundA large body of evidence highlights the importance of genetic variants in the development of psychiatric and metabolic conditions. Among these, the TaqIA polymorphism is one of the most commonly studied in psychiatry. TaqIA is located in the gene that codes for the ankyrin repeat and kinase domain containing 1 kinase (Ankk1) near the dopamine D2 receptor (D2R) gene. Homozygous expression of the A1 allele correlates with a 30% to 40% reduction of striatal D2R, a typical feature of addiction, overeating, and other psychiatric pathologies. The mechanisms by which the variant influences dopamine signaling and behavior are unknown. MethodsHere, we used transgenic and viral-mediated strategies to reveal the role of Ankk1 in the regulation of activity and functions of the striatum. ResultsWe found that Ankk1 is preferentially enriched in striatal D2R-expressing neurons and that Ankk1 loss of function in the dorsal and ventral striatum leads to alteration in learning, impulsivity, and flexibility resembling endophenotypes described in A1 carriers. We also observed an unsuspected role of Ankk1 in striatal D2R-expressing neurons of the ventral striatum in the regulation of energy homeostasis and documented differential nutrient partitioning in humans with or without the A1 allele. ConclusionsOverall, our data demonstrate that the Ankk1 gene is necessary for the integrity of striatal functions and reveal a new role for Ankk1 in the regulation of body metabolism.

Associations among SNPs in two addictive genes, food addiction, and antioxidant markers in recreationally active young women.

Introduction: food addiction is associated with genetic polymorphisms and decreased antioxidant intake. Objectives: this study determined the associations among food addiction, dopamine receptor 2 (DRD2) and toll-interleukin 1 receptor (TIR) domain-containing adaptor protein (TIRAP rs625413) gene polymorphisms, antioxidant capacities, and zinc levels among recreationally active Turkish women. Methods: the Yale Food Addiction Scale was used to evaluate the food addiction status. Serum antioxidant capacities and zinc levels were evaluated by blood analyses. Deoxyribonucleic acid (DNA) extraction was performed using peripheral blood leukocytes, and the polymorphism status of the DRD2 Taq 1A and TIRAP genes was investigated using a commercial kit. Results: the frequencies of the heterozygous genotypes of DRD2 Taq 1A and TIRAP were 23.1 % and 31.4 %, respectively, and the frequency of risk allele homozygous genotypes was 3.2 %. Most participants (94.4 %) had a nonpolymorphic/wild (CC) genotype in both genes; however, 11.5 % of the participants had a food addiction. The differences between serum antioxidant capacities, zinc levels, and body mass indices of those with and without food addiction were statistically significant. However, there were no differences in the serum zinc and antioxidant levels among the different genotypes. Conclusion: food addiction in young Turkish women was not associated with DRD2 Taq 1A or TIRAP polymorphisms but was associated with serum antioxidant capacities and zinc levels. Further studies on different loci of the same genes or genotypes of different genes with larger sample sizes are warranted.

The ANKK1/DRD2 gene TaqIA polymorphism (rs1800497) is associated with the severity of extrapyramidal side effects of haloperidol treatment in CYP2D6 extensive metabolizers with schizophrenia spectrum disorders.

Extrapyramidal symptoms (EPS) are one of the most prominent side effects of haloperidol. Variability of EPS severity may be associated with the genetic factors, affecting both haloperidol pharmacokinetics (e.g., CYP2D6) and pharmacodynamics (e.g., DRD2, ANKK1). We conducted a 3-week prospective study to investigate the associations of ANKK1/DRD2 TaqIA (rs1800497), DRD2-141C Ins/Del (rs1799732) polymorphisms and CYP2D6 metabolic phenotype on the efficacy of haloperidol treatment and severity of EPS in patients with schizophrenia spectrum disorders. In total, 57 inpatients with schizophrenia spectrum disorders (24 (42.1%)) females; age-46.7 (11.8) years (M(SD)) of European ancestry were enrolled. BARS and SAS scales were used to assess EPS. PANSS and CGI scales- to assess the efficacy of haloperidol treatment. Genotyping was performed by real-time PCR. CYP2D6 metabolic phenotype was predicted by the CYP2D6 *3, *4, *5, *6, *9, *10, *41 and xN genotypes. Minor C allele of TaqIA was associated with higher scores of BARS (p=0.029) and SAS (p=0.024) on day 21 and minor Del allele of-141C Ins/Del- with more prominent clinical improvement by CGI scale (p=0.007) but not by PANSS. These differences were observed only in extensive CYP2D6 metabolizers, although no associations with the metabolic type itself were found. General linear model showed that the combination of TaqIA genotype and metabolic type was significantly associated with BARS score on day 21 (p=0.013). Our results highlight the importance of using both pharmacokinetic and pharmacodynamic genetic markers for predicting haloperidol treatment response to personalize schizophrenia spectrum disorders treatment.

Are COMT Val158Met (rs4680), DRD2 TaqIA (rs1800497), and BDNF Val66Met (rs6265) polymorphisms associated with executive functions performance at rest and during physical exercise?

Executive functions (EFs) encompass a wide array of cognitive processes, which appear to be influenced by genetic variants of the COMT, DRD2/ANKK1, and BDNF polymorphisms. The present study aimed to investigate whether COMT Val158Met (rs4680), DRD2/ANKK1 (rs1800497), and BDNF Val66Met (rs6265) polymorphisms were associated with EFs assessed at rest and during moderate acute physical exercise. Sixty physically active individuals underwent four laboratory visits. First, they filled out the pre-exercise survey, researchers collected their anthropometric data, and then performed a maximal cardiopulmonary exercise test. In the second and third sessions, participants performed EFs test in a randomized order: while the individual was seated on a cycle ergometer without pedaling (i.e., rest condition); and during physical exercise (pedaling for 30 minutes at moderate intensity before starting the EFs test during exercising). On the fourth day, blood samples were drawn. Our results showed that the response time of the COMT Val homozygotes group was significantly shorter than the COMT Met-carrier group [t(39.78) = 2.13, p = .039,d = 0.56] at rest condition. No significant association was found for the other analyses (DRD2/ANKK1 and BDNF). In conclusion, the present study suggests that COMT Val158Met (rs4680) polymorphisms may be associated with EFs at rest condition. However, further studies are needed to validate this association.

The Personality Traits and P300 of Offspring of Parents With Alcohol Dependence Differ Depending on Current Risky Drinking: A Preliminary Case-Control Study.

AimsThe aim of this study was to investigate the personality traits, and P300 component in the offspring of parents with alcohol dependence (OPAD) currently engaged in risky drinking and those not engaged in risky drinking, and to further explore the correlates of problematic alcohol use.MethodsA case-control study was conducted according to the cutoff of the Alcohol Use Disorder Identification Test (AUDIT). The frequency of the TaqIA polymorphism of the dopamine receptor D2 gene associated with alcohol dependence was compared between the two OPAD groups. Tridimensional Personality Questionnaire (TPQ), The Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST), and the MINI-International Neuropsychiatric Interview (M.I.N.I.) were measured or interviewed in OPAD not engaged in risky drinking (resilient; n = 35) and those currently engaged in risky drinking (vulnerable; n = 20). P300 was measured to test the possible electrophysiological differences. The correlates of alcohol use were analyzed.ResultsVulnerable OPAD showed higher novelty seeking subscale scores (NS4; 4.45 ± 2.012 vs. 3.31 ± 1.728, P < 0.05) and harm avoidance subscale scores (HA4; 5.3 ± 2.319 vs. 3.66 ± 2.461, P < 0.05) than resilient OPAD, while the total scores of each dimension showed no significant difference. OPAD engaged in risky drinking showed more tobacco use than OPAD resistant to risky drinking. OPAD with risky drinking showed a shorter P300 latency than resilient OPAD on Fz electrodes. AUDIT scores of OPAD were correlated with P300 latency.ConclusionsP300 differed between OPAD with and without risky drinking and alcohol use was associated with P300 latency, indicating that P300 may be used in the early detection of vulnerable OPAD and early intervention in the future.

The effect of parenting styles on depressive symptoms among Chinese college students: The role of subjective well-being and Taq1A polymorphism

The effect of parenting styles on depressive symptoms among Chinese college students: The role of subjective well-being and Taq1A polymorphism

Clustering of Parkinson subtypes reveals strong influence of DRD2 polymorphism and gender

Most classification approaches for idiopathic Parkinson’s disease subtypes primarily focus on motor and non-motor symptoms. Besides these characteristics, other features, including gender or genetic polymorphism of dopamine receptors are potential factors influencing the disease’s phenotype. By utilizing a kmeans-clustering algorithm we were able to identify three subgroups mainly characterized by gender, DRD2 Taq1A (rs1800497) polymorphism—associated with changes in dopamine signaling in the brain—and disease progression. A subsequent regression analysis of these subgroups further suggests an influence of their characteristics on the daily levodopa dosage, an indicator for medication response. These findings could promote further enhancements in individualized therapies for idiopathic Parkinson’s disease.

DRD2 Taq1A Polymorphism-Related Brain Volume Changes in Parkinson's Disease: Voxel-Based Morphometry.

Taq1A polymorphism is a DRD2 gene variant located in an exon of the ANKK1 gene and has an important role in the brain's dopaminergic functions. Some studies have indicated that A1 carriers have an increased risk of developing Parkinson's disease (PD) and show poorer clinical performance than A2 homo carriers. Previous studies have suggested that A1 carriers had fewer dopamine D2 receptors in the caudate and increased cortical activity as a compensatory mechanism. However, there is little information about morphological changes associated with this polymorphism in patients with PD. The study's aim was to investigate the relationship between brain volume and Taq1A polymorphism in PD using voxel-based morphometry (VBM). Based on Taq1A polymorphism, 103 patients with PD were divided into two groups: A1 carriers (A1/A1 and A1/A2) and A2 homo carriers (A2/A2). The volume of the left prefrontal cortex (PFC) was significantly decreased in A2 homo carriers compared to A1 carriers. This finding supports the association between Taq1A polymorphism and brain volume in PD and may explain the compensation of cortical function in A1 carriers with PD.

P.0575 DRD2/ANKK1 Taq1A polymorphism is associated with elevated serum prolactin levels during haloperidol treatment in schizophrenia spectrum disorders patients

P.0575 DRD2/ANKK1 Taq1A polymorphism is associated with elevated serum prolactin levels during haloperidol treatment in schizophrenia spectrum disorders patients

Single Nucleotide Polymorphism rs1800497 in Risperidone and Aripiprazole Therapy for Schizophrenia Patients

Schizophrenia is a variable of psychopathologic syndrome involving cognition, emotion, perception, and other behavioral aspects. Therapies on schizophrenia is solely based on history of mental illnesses and mental status. Schizophrenia affecting 1.1 million persons globally in 2017; 70.8% of them happened in 25-55 years old. This study was conducted in mental hospital in Palembang, Indonesia. Blood samples was taken from clinically diagnosed schizophrenia patients (20 patients taking aripiprazole and 60 patients taking risperidone) under therapy. DNA was extracted using Chelex 100 method and digested using Taq1 enzyme. DNA was electrophoresized and visualized. CC allele was found in 10% of patients taking aripiprazole and 11.67% patients taking risperidone. CT allele was found in 70% patients taking aripiprazole and 76.67% patients taking risperidone. TT allele was found in 20% patients taking aripiprazole and 11.67% patients taking risperidone. ANKK1 Taq1A polymorphism in schizophrenia patients shows different therapeutic response with worse therapeutic response compared to patients with normal allele.

BDNF Val66Met polymorphism is associated with negative symptoms in early-onset schizophrenia spectrum and other psychotic disorders

Background and ObjectivesTo investigate the clinical characteristics of adolescents with early-onset full psychotic disorders either with Brain-derived neurotrophic factor (BDNF) Val66Met (rs6265) or DRD2/ANKK1 Taq1A (rs1800497) polymorphisms. Method101 cases with early-onset schizophrenia (EOS) or other psychotic spectrum disorders (SSD) and 150 healthy controls were included in the current study. Using the Positive and Negative Symptom Scale (PANSS), patient subgroups were compared for their psychotic symptoms, age-onset, duration of untreated illness, and family history of psychiatric disorders. The real-time polymerase chain reaction (RT-PCR) was implemented for genotyping procedures. ResultsStudy groups and patient subgroups were similar regarding their sociodemographic characteristics (16.4 ± 2.6 years, 62.2% male for all participants). Results did not reveal any difference between patients and healthy controls for DRD2/ANKK1 Taq1A and BDNF Val66Met genotypes. Patients with A1A2 (Gly/Lys) allele reported higher rates of substance use compared to A2A2 (Glu/Glu) counterparts. Other clinical variables were found similar. EOS/SSD group with Val66Met heterozygote allele revealed lower levels of negative symptoms than Val/Val homozygotes. Conversely, the age onset of full psychotic disorder, total positive symptom score, and total general psychopathology score of PANSS were found comparable between Val/Met and Val/Val groups. In the logistic regression model, Glu/Lys genotypes remained significant for the presence of substance use. ConclusionThe interaction between substance use and the DRD2 gene should be investigated for the development of early-onset psychotic disorders. BDNF Val66Met polymorphism also could be a disease-modifying factor for the presence of negative symptoms.

Investigating the association between common DRD2/ANKK1 genetic polymorphisms and schizophrenia: a meta-analysis

Genetic factors play an important role in the pathogenesis of schizophrenia. Dysregulations in the dopaminergic system have long been known to play an influential role in the development of this disorder. Although a large number of studies have investigated the association between genetic polymorphisms in the genes involved in this system and the risk of schizophrenia, the results have been inconsistent. In this meta-analysis, we searched for publications in Ovid Medline, Embase, Web of Science (science citation index expanded), and PsycNET for articles published until January 2020. We identified case-control studies investigating the association between four common genetic polymorphisms (rs6277, rs1799732, rs1800497, and rs1801028) and the risk of schizophrenia. The studies were subsequently selected according to the predefined inclusion and exclusion criteria. The data extraction was conducted according to the PRISMA guidelines.We also assessed the quality of the studies and investigated publication bias using funnel plot and Egger's regression test. The association analysis was conducted in allelic, dominant, and recessive genetic models. Subsequently, bioinformatics analysis of the effect of the polymorphisms found to be significantly associated with schizophrenia on protein stability, posttranslational modifications, and 3D protein structure was conducted. This meta-analysis showed that Taq1A (allelic model: OR, 0.856, 95% CI, 0.734-0.998) has a protective effect against the development of schizophrenia. Further, it was found that this variant may decreaseANKK1protein stability. Further, this polymorphism was found to lead to the gain of modifications sites for ubiquitination (Ubi. score =-1.894) and methylation (Meth. score =-0.834). Several genetic factors contribute to the susceptibility of schizophrenia. The updated knowledge emerging from this meta-analysis showing the protective effect of rs1800497 polymorphism (Taq1A) can shed light on the role of Taq1A polymorphism in the susceptibility to schizophrenia and also pave way for further functional studies investigating the role of ANKK1 protein in the pathogenesis of schizophrenia.

Motivational learning biases are differentially modulated by genetic determinants of striatal and prefrontal dopamine function

Dopaminergic neurotransmission plays a pivotal role in appetitively motivated behavior in mammals, including humans. Notably, action and valence are not independent in motivated tasks, and it is particularly difficult for humans to learn the inhibition of an action to obtain a reward. We have previously observed that the carriers of the DRD2/ANKK1 TaqIA A1 allele, that has been associated with reduced striatal dopamine D2 receptor expression, showed a diminished learning performance when required to learn response inhibition to obtain rewards, a finding that was replicated in two independent cohorts. With our present study, we followed two aims: first, we aimed to replicate our finding on the DRD2/ANKK1 TaqIA polymorphism in a third independent cohort (N = 99) and to investigate the nature of the genetic effects more closely using trial-by-trial behavioral analysis and computational modeling in the combined dataset (N = 281). Second, we aimed to assess a potentially modulatory role of prefrontal dopamine availability, using the widely studied COMT Val108/158Met polymorphism as a proxy. We first report a replication of the above mentioned finding. Interestingly, after combining all three cohorts, exploratory analyses regarding the COMT Val108/158Met polymorphism suggest that homozygotes for the Met allele, which has been linked to higher prefrontal dopaminergic tone, show a lower learning bias. Our results corroborate the importance of genetic variability of the dopaminergic system in individual learning differences of action–valence interaction and, furthermore, suggest that motivational learning biases are differentially modulated by genetic determinants of striatal and prefrontal dopamine function.