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Serotonin Transporter Gene (serotonin + transporter_gene)
Selected AbstractsThe serotonin transporter 5-HTTPR polymorphism is associated with current and lifetime depression in persons with chronic psychotic disordersACTA PSYCHIATRICA SCANDINAVICA, Issue 2 2009J. Contreras Objective:, Variation in the serotonin transporter gene (SLC6A4) promoter region has been shown to influence depression in persons who have been exposed to a number of stressful life events. Method:, We evaluated whether genetic variation in 5-HTTLPR, influences current depression, lifetime history of depression and quantitative measures of depression in persons with chronic psychotic disorders. This is an association study of a genetic variant with quantitative and categorical definitions of depression conducted in the southwest US, Mexico and Costa Rica. We analyzed 260 subjects with a history of psychosis, from a sample of 129 families. Results:, We found that persons carrying at least one short allele had a statistically significant increased lifetime risk for depressive syndromes (P < 0.02, odds ratio 2.18, 95% CI 1.10,4.20). Conclusion:, The ,ss' or ,sl' genotype at the 5-HTTLPR promoter polymorphic locus increases the risk of psychotic individuals to develop major depression during the course of their illness. [source] An international multicenter association study of the serotonin transporter gene in persistent ADHDGENES, BRAIN AND BEHAVIOR, Issue 5 2010E. T. Landaas Attention deficit hyperactivity disorder (ADHD) is a common behavioral disorder affecting children and adults. It has been suggested that gene variants related to serotonin neurotransmission are associated with ADHD. We tested the functional promoter polymorphism 5-HTTLPR and seven single nucleotide polymorphisms in SLC6A4 for association with ADHD in 448 adult ADHD patients and 580 controls from Norway. Replication attempts were performed in a sample of 1454 Caucasian adult ADHD patients and 1302 controls from Germany, Spain, the Netherlands and USA, and a meta-analysis was performed also including a previously published adult ADHD study. We found an association between ADHD and rs140700 [odds ratio (OR ) = 0.67; P = 0.01] and the short (S) allele of the 5-HTTLPR (OR = 1.19; P = 0.06) in the Norwegian sample. Analysis of a possible gender effect suggested that the association might be restricted to females (rs140700: OR = 0.45; P = 0.00084). However, the meta-analysis of 1894 cases and 1878 controls could not confirm the association for rs140700 [OR = 0.85, 95% confidence interval (CI) = 0.67,1.09; P = 0.20]. For 5-HTTLPR, five of six samples showed a slight overrepresentation of the S allele in patients, but meta-analysis refuted a strong effect (OR = 1.10, 95% CI = 1.00,1.21; P = 0.06). Neither marker showed any evidence of differential effects for ADHD subtype, gender or symptoms of depression/anxiety. In conclusion, our results do not support a major role for SLC6A4 common variants in persistent ADHD, although a modest effect of the 5-HTTLPR and a role for rare variants cannot be excluded. [source] Serotonergic genes modulate amygdala activity in major depressionGENES, BRAIN AND BEHAVIOR, Issue 7 2007U. Dannlowski Serotonergic genes have been implicated in the pathogenesis of depression probably via their influence on neural activity during emotion processing. This study used an imaging genomics approach to investigate amygdala activity in major depression as a function of common functional polymorphisms in the serotonin transporter gene (5-HTTLPR) and the serotonin receptor 1A gene (5-HT1A -1019C/G). In 27 medicated patients with major depression, amygdala responses to happy, sad and angry faces were assessed using functional magnetic resonance imaging at 3 Tesla. Patients were genotyped for the 5-HT1A -1019C/G and the 5-HTTLPR polymorphism, including the newly described 5-HTT-rs25531 single nucleotide polymorphism. Risk allele carriers for either gene showed significantly increased bilateral amygdala activation in response to emotional stimuli, implicating an additive effect of both genotypes. Our data suggest that the genetic susceptibility for major depression might be transported via dysfunctional neural activity in brain regions critical for emotion processing. [source] No Influence of 5-HTTLPR Gene Polymorphism on Migraine Symptomatology, Comorbid Depression, and ChronificationHEADACHE, Issue 3 2010Thomas Wieser MD (Headache 2010;50:420-430) Background., The serotonergic system is thought to play an important role for mediating susceptibility to migraine and depression, which is frequently found comorbid in migraine. The functional polymorphism in the serotonin transporter gene linked polymorphic region (5-HTTLPR/SLC6A4) was previously associated with attack frequency and, thus, possibly with chronification. Objective., We hypothesized that patients with the "s" allele have higher attack frequency and, paralleling results in depression research, higher scores of depression. Methods., Genetic analysis of the SLC6A4 44 bp insertion/deletion polymorphism (5-HTTLPR) was performed in 293 patients with migraine with and without aura. Self-rating questionnaires were used for assessment of depression. Results., Multinomial logistic regression analysis found no evidence for association of the 5-HTTLPR polymorphism with either depression or migraine attack frequency. Conclusion., We were not able to demonstrate any influence of the serotonin transporter 5-HTTLPR polymorphism on migraine phenomenology (attack frequency or comorbid depression), thereby excluding this variant to be a common genetic denominator for chronic migraine and depression. [source] Serotonin Transporter Protein Polymorphism and Harm Avoidance Personality in Migraine without AuraHEADACHE, Issue 6 2006Jeong Wook Park MD Objective.,To investigate polymorphisms in the serotonin transporter protein gene and harm avoidance personality dimension in patients with migraine without aura (MWOA). Background.,The serotonin transporter protein is a key modulator of serotonergic synaptic neurotransmission. Two polymorphic regions of the gene for serotonin transporter protein have been found, and are associated with variations in the functional activity of serotonin caused by differing transcriptional efficiency. The harm avoidance (HA) personality trait may also be heritable and associated with altered serotonergic neurotransmitter activity. Design.,We amplified the polymorphism in the promoter of serotonin transporter protein (5-HTTLPR) and the variable number of tandem repeats polymorphism within intron 2 (VNTR) using the polymerase chain reaction and performed genotype polymorphism analyses in 97 patients with MWOA and 100 healthy controls. We investigated serotonin-related personality traits by evaluating the HA personality dimension using a tridimensional questionnaire. Results.,The genotype frequencies and allele distributions of 5-HTTLPR did not differ between patients with MWOA and controls. The VNTR genotype STin2.12/STin2.12 was significantly more common in patients with MWOA (90%) than in controls (77%; P= .017). Patients with MWOA also had HA scores (21.9 ± 6.4) significantly higher than those of controls (16.3 ± 6.1; P < .001). Conclusions.,Serotonergic activity might be involved in the development of MWOA and VNTR of serotonin transporter gene might be one of the genetically contributing factors. [source] Association of serotonin transporter gene-linked polymorphic region and variable number of tandem repeat polymorphism of the serotonin transporter gene in lichen simplex chronicus patients with psychiatric statusINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2008Necmettin Kirtak MD Background, The serotonin (5-hydroxytryptamine; 5-HT) is a key neurotransmitter in the central nervous system and a responsible mediator for the itch. Dysregulation of serotonergic pathways has been implicated in the pathogenesis of many complex neuropsychiatric diseases. Objectives, The purpose of this study was to evaluate the relationship between lichen simplex chronicus and dysfunction and serotonin transporter (5-HTT) gene polymorphism. Methods, Thirty-nine patients with lichen simplex chronicus and 61 healthy control subjects were examined. Results, The results for the patients and control subjects were not significantly different (P > 0.05) in long/long (L/L) and long/short (L/S) genotypes of 5-HTT gene-linked polymorphic region (HTTLPR) polymorphism, but short/short S/S genotype was lower in lichen simplex chronicus patients (17.9%) than in controls (42.6%). This difference was statistically significant (P = 0.028). The results for the patients and control subjects were not significantly different in 12/12, 10/12 and 10/10 genotypes of variable number of tandem repeat (VNTR) polymorphism (P > 0.05). Beck depression inventory (BDI) scores and symptom checklist-90-revised (SCL-90) psychotic subscale were overrepresented significantly in the 12/12 genotypes than 10/12 genotypes. State and Trait Anxiety Inventory tests (STAI-I and -II) point averages were not statistically significant (P > 0.05) Conclusion, S/S genotypes of HTTLPR polymorphism in the 5-HTT gene may be related to lichen simplex chronicus and that patients who have 12/12 genotypes of VNTR polymorphism may be affected psychiatrically. [source] An investigation of associations between alcohol use disorder and polymorphisms on ALDH2, BDNF, 5-HTTLPR, and MTHFR genes in older Korean menINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 5 2010Sangmoon Shin Abstract Background This study aimed to investigate the association of alcohol use disorder (AUD) with four candidate genes in older Korean men: aldehyde dehydrogenase 2 (ALDH2, 1/2), brain-derived neurotrophic factor (BDNF, val66met), serotonin transporter gene linked polymorphic region (5- HTTLPR, s/l), and methylenetetrahydrofolate reductase (MTHFR, c.677C,>,T). Methods A community sample of 300 men aged 65 or over were categorized into 68 subjects with AUD and 232 controls according to clinical examinations and DSM-IV criteria. Genotype distributions and allele frequencies were compared. Results Men with AUD had significantly higher ALDH2*1 and BDNF met allele frequencies compared to controls (p -values,<,0.05). No significant differences in genotype or allele frequencies were found for 5- HTTLPR or MTHFR (p -values,>,0.3). Conclusions AUD was associated with ALDH2*1 and BDNF met alleles in older Korean men. The first is consistent with previous research and likely to be explained by a protective effect of unpleasant symptoms following alcohol consumption associated with ALDH2*2. The second finding is novel and might be accounted for by BDNF -mediated serotonin or dopamine pathways. However, given the relatively small sample size, the results should be regarded as preliminary and requiring independent replication. Copyright © 2009 John Wiley & Sons, Ltd. [source] Serotonin receptors antagonistically modulate Caenorhabditis elegans longevityAGING CELL, Issue 4 2007Hana Murakami Summary The neurotransmitter serotonin has been implicated in affecting the variation of longevity in natural Drosophila populations and age-related diseases in mammals. Based on these observations, it has been predicted that serotonin signal, perhaps at levels of serotonin biosynthesis, may control lifespan. Here, we investigated a variety of mutations in serotonin-signal genes, including serotonin biosynthesis genes, a serotonin transporter gene, and serotonin receptor genes. Despite this prediction, mutations in the serotonin biosynthesis genes had little or modest effects on lifespan, while the mod-5 mutation with increased availability of serotonin caused a modest life-shortening effect. In contrast, a deletion mutation of the ser-1 serotonin receptor gene increased longevity by up to 46%, likely through the insulin/insulin-like growth factor 1 pathway. This result suggests an interaction between the serotonin pathway and the insulin/insulin-like growth factor 1 pathway. A deletion mutation of another serotonin receptor gene, ser-4, shortened early to mid lifespan. The results suggest that serotonin signal antagonistically modulates longevity through different serotonin receptors. This study may indicate serotonin receptors as a potential target for antigeric interventions. [source] Characterization of a Functional Polymorphism in the 3, UTR of SLC6A4 and its Association With Drinking IntensityALCOHOLISM, Issue 2 2009Chamindi Seneviratne Background:, The propensity for severe drinking is hypothesized to be regulated by differential expression of serotonin transporter gene (SLC6A4) in the human brain. The SLC6A4 promoter region 5-HTTLPR has been examined previously as a candidate polymorphic variant associated with severe drinking. In this study, we investigated whether other SLC6A4 single nucleotide polymorphisms (SNPs) are associated with drinking intensity among treatment-seeking alcoholics and whether these polymorphic variants result in differential SLC6A4 expression levels. Methods:, We analyzed associations of drinking intensity in 275 (78.5% male) treatment-seeking alcoholics of Caucasian and Hispanic origin, with 6 SLC6A4 polymorphisms. Next, to examine the functionality of the SNP that showed a significant association with drinking intensity, we transfected the 2 alleles of rs1042173 into HeLa cell cultures and measured serotonin transporter mRNA and protein expression levels by using qRT-PCR and western blotting techniques. Results:, One of the 6 polymorphisms we examined, rs1042173 in the 3, untranslated region (3,-UTR) of SLC6A4, showed a significant association with drinking intensity. The G allele carriers for rs1042173 were associated with significantly lower drinking intensity (p = 0.0034) compared to T-allele homozygotes. In HeLa cell cultures, the cells transfected with G allele showed a significantly higher mRNA and protein levels than the T allele-transfected cells. Conclusion:, These findings suggest that the allelic variations of rs1042173 affect drinking intensity in alcoholics possibly by altering serotonin transporter expression levels. This provides additional support to the hypothesis that SLC6A4 polymorphisms play an important role in regulating propensity for severe drinking. [source] Comorbidity of Alcohol Dependence With Attention-Deficit Hyperactivity Disorder: Differences in Phenotype With Increased Severity of the Substance Disorder, but Not in Genotype (Serotonin Transporter and 5-Hydroxytryptamine-2c Receptor)ALCOHOLISM, Issue 10 2003Monika Johann Background: Nearly 50% of subjects with continuing symptoms of attention-deficit hyperactivity disorder (ADHD) in adulthood have been reported to show a comorbid substance use disorder. Both ADHD and alcohol dependence have a high genetic load and might even share overlapping sources of genetic liability. Recently, the functional relevant polymorphism within the promoter region of the serotonin transporter gene (5-HTT) and the 5-hydroxytryptamine-2c (5-HT2c) receptor Cys23Ser have been proposed as candidate genes for both entities. Methods: We investigated phenotype and 5-HTT/5-HT2c genotype characteristics in 314 alcoholics of German descent. Results: There was no significant difference in 5-HTT genotype or 5-HT2c allele distribution between alcoholics and matched controls. Sixty-seven alcoholics fulfilled DSM-IV criteria of ADHD with ongoing symptoms in adulthood and had a Wender Utah Rating Scale score greater than 90. Thirty had ADHD plus antisocial personality disorder. The subgroup of alcoholics with ADHD (ADHD+) showed a significantly higher daily and record ethanol intake per month, an earlier age at onset of alcohol dependence, and a higher frequency of suicidal ideation, court proceedings, and antisocial personality disorder. In our sample, more than 50% of type 2 alcoholics according to Cloninger consist of the ADHD+ and/or antisocial personality disorder-positive subjects. There were no differences in 5-HTT genotype or 5-HT2c allele distribution between the ADHD+ subgroups and alcoholics without comorbidity and matched controls, respectively. Conclusions: Comorbidity of alcoholism and ADHD forms a distinct phenotype that shows an increased severity of the substance disorder. This phenotype contributes substantially to the so-called type 2 alcoholics according to Cloninger. In our sample, the functional relevant 5-HTT promoter and the 5-HT2c receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and alcohol dependence. [source] Association of DRD3 and GRIN2B with impulse control and related behaviors in Parkinson's disease,MOVEMENT DISORDERS, Issue 12 2009Jee-Young Lee MD Abstract We aimed to assess whether allelic variants of dopamine receptor, glutamate receptor, and serotonin transporter genes are associated with the appearance of impulse control and related behaviors (ICRB) in Parkinson's disease (PD) with dopamine replacement therapy (DRT). We surveyed ICRB in consecutive Korean patients with PD who were treated with stable DRT using modified Minnesota Impulsive Disorders Interview over a period of 4 months. In the 404 patients who completed the interview and the 559 Korean healthy normal controls, genotyping was performed for variants of the DRD3 p.S9G, DRD2Taq1A, GRIN2B c.366C>G, c.2664C>T and c.-200T>G, and the promoter region of the serotonin transporter gene (5-HTTLPR). Behavioral abnormalities suggestive of ICRB including compulsive buying, gambling, sexual behavior and eating, and punding, were present in 14.4% of the patients. Variants of DRD2 and 5-HTTLPR were not associated with the risk of developing ICRB. However, the AA genotype of DRD3 p.S9G and the CC genotype of GRIN2B c.366C>G were more frequent in patients with ICRB than in nonaffected patients (odds ratio [OR] = 2.21, P = 0.0094; and 2.14, P = 0.0087, after adjusting for age and sex). After controlling for clinical variables in the multivariate analysis, carriage of either AA genotype of DRD3 or CC genotype of GRIN2B was identified as an independent risk factor for ICRB (adjusted OR: 2.57, P = 0.0087). Variants of DRD3 p.S9G and GRIN2B c.366C>G may be associated with the appearance of ICRB in PD. © 2009 Movement Disorder Society [source] Serotonin transporter gene polymorphism and psychiatric disorders in NF1 patientsAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 8 2001Frank Bellivier Abstract Neurofibromatosis type 1 (NF1) is an autosomal-dominant genetic disease characterized by a broad clinical expression. Comorbid affective disorders, anxiety disorders, and suicide are frequently observed during NF1. The promoter marker (5-HTTLPR) of the serotonin transporter gene (5-HTT) has been shown to be associated with major affective disorders, anxiety-related trait, and more recently with suicidal behavior. This gene is adjacent to the NF1 gene, raising the question of the implication of the 5-HTT gene in the psychiatric comorbidity during NF1. Eighty-eight patients with NF1 and 184 screened controls were typed for the 5-HTTLPR. No deviation from the Hardy-Weinberg equilibrium in patients was observed. In addition, allele and genotype frequencies were similar in the two groups. Our data do not support the implication of the 5-HTT gene in the psychiatric comorbidities of NF1. © 2001 Wiley-Liss, Inc. [source] Loneliness in adolescence: gene × environment interactions involving the serotonin transporter geneTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 7 2010Eeske Van Roekel Background:, Loneliness is assumed to peak in early adolescence and to decrease throughout middle and late adolescence, but longitudinal confirmation of this tendency is lacking. Behavioral genetic studies with twin designs have found a significant genetic component for loneliness in children and adults, but no molecular genetic studies have been conducted to reveal the functional polymorphisms involved. Methods:, Associations among the serotonin transporter gene (5-HTTLPR), sex, parental support, and loneliness were examined in a longitudinal study spanning five annual waves (N = 306). Results:, Using latent growth curve modeling (LGCM), loneliness was found to be highest in early adolescence and slowly declined throughout adolescence. The 5-HTTLPR genotype was related to the development of loneliness, in that short allele carriers remained stable in loneliness over time, whereas adolescents with the long-long genotype decreased in loneliness. Interactions were found between maternal support and 5-HTTLPR genotype, showing that adolescents who perceived little support from their mothers and carried a short allele were at increased risk for developing loneliness. Conclusions:, Our study is the first to chart adolescent loneliness longitudinally and to examine the genetic underpinnings of loneliness. Our results contribute to a further understanding of the environmental and genetic basis of loneliness. Replication of our results is needed in both population-based and clinical samples. [source] Interplay of genes and early mother,child relationship in the development of self-regulation from toddler to preschool ageTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 11 2009Grazyna Kochanska Background:, A broad capacity for deliberate self-regulation plays a key role in emotion regulation. This longitudinal investigation from infancy to preschool age examines genotype by environment (G × E) interaction in the development of self-regulation, using molecular measures of children's genotypes and observed measures of the quality of early mother,child relationship, as reflected in attachment organization in infancy. Methods:, In 89 children, we assessed the polymorphism in the serotonin transporter gene (5-HTTLPR, ss/sl vs. ll allele status), security of attachment to mothers at 15 months in the Strange Situation, and children's ability for self-regulation at 25, 38, and 52 months, using behavioral batteries of tasks that called for deliberately suppressing a dominant response and performing instead a sub-dominant response. Results:, There was a robust G × E interaction between genetic risk and the quality of early relationship. Among children who carried a short 5-HTTLPR allele (ss/sl,), those who were insecurely attached developed poor regulatory capacities, but those who were securely attached developed as good regulatory capacities as children who were homozygotic for the long allele (ll,). There was no effect of security for ll homozygotes. Conclusions:, Those findings, consistent with diathesis-stress model, bridge research on self-regulation in typically developing children with research on non-human primates and research on psychopathology. They also indicate that a secure attachment relationship can serve as a protective factor in the presence of risk conferred by a genotype. [source] Genetic and attachment influences on adolescents' regulation of autonomy and aggressivenessTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 11 2009Peter Zimmermann Background:, Adolescence is a time when intense emotions are elicited within the parent,adolescent relationship, often when autonomy subjectively is endangered. As emotion dysregulation is one of the risk processes for the development of psychopathology, adolescence may be perceived as a highly sensitive period for maladjustment. Inter-individual differences in emotionality and emotion regulation have been shown to be influenced or moderated by molecular genetic differences in the serotonin transporter gene (5-HTT) and by attachment patterns. We investigated whether both the 5-HTT and attachment are associated with emotionality and emotion regulation in an observed adolescent,mother interaction and the personality traits aggressiveness and anxiety in adolescence. Methods:, Ninety-one adolescents at age 12 were observed in interaction with their mothers during a standardized emotion-eliciting social task to assess emotionality and emotion regulation in relation to autonomy. Adolescents' aggressiveness and anxiety were assessed by mother report. Concurrent attachment quality was determined by an attachment interview. DNA samples were collected in order to assess the 5-HTTLPR, a repeat polymorphism in the promoter region of the serotonin transporter gene. Results:, While the short allele of the serotonin transporter gene was associated with a higher overall rate of autonomy behaviors, attachment security was related to more agreeable and less hostile autonomy. A significant interaction revealed a moderating effect of attachment security. Carriers of the short version of the 5-HTTLPR showed more agreeable autonomy when they had a secure attachment behavior strategy but showed more hostile autonomy when they were insecurely attached. Carriers of the short version of the 5-HTTLPR and insecurely attached adolescents were rated as more aggressive. Conclusions:, The study suggests a gene,attachment interaction in adolescents where the adolescent's attachment status moderates a genetically based higher negative reactivity in response to threats to autonomy in social interactions. [source] Association between brain-derived neurotrophic factor gene and a severe form of bipolar disorder, but no interaction with the serotonin transporter geneBIPOLAR DISORDERS, Issue 5 2008Ilona Vincze Background:, Recent data suggest that brain-derived neurotrophic factor (BDNF) and the serotonergic system are involved and interact in major depressive disorder and suicidal behavior (SB). Several family and population-based studies have reported associations between the BDNF gene and serotonin-related genes, specifically the serotonin transporter (5HTT) gene, with bipolar disorder (BD) and SB. However, despite the fact that gene-by-gene interaction between BDNF and 5HTT has been demonstrated in monoamine deficiencies in animals, this kind of interaction has never been tested in humans. Our hypothesis is that some BDNF and 5HTT polymorphisms might confer increased risk for BD and SB and that both genes may interact with each other. Methods:, To test this hypothesis, we genotyped the most common BDNF polymorphisms, G196A (Val66Met), A-633T and BDNF-LCPR, as well as 5HTT (5HTT-LPR), in 447 BD patients and 370 controls. Results:, We replicated the association previously reported between BDNF G196A (Val66Met) polymorphism and BD. We also observed a correlation between the number of G196 alleles and short alleles of 5HTT-LPR and the severity of SB in BD. However, we found no significant interaction between these two markers. Conclusions:, These results suggest that BDNF G196A as well as 5HTT-LPR polymorphisms confer risk for SB in BD, but we did not observe any evidence for an interaction between them. [source] Association of DRD3 and GRIN2B with impulse control and related behaviors in Parkinson's disease,MOVEMENT DISORDERS, Issue 12 2009Jee-Young Lee MD Abstract We aimed to assess whether allelic variants of dopamine receptor, glutamate receptor, and serotonin transporter genes are associated with the appearance of impulse control and related behaviors (ICRB) in Parkinson's disease (PD) with dopamine replacement therapy (DRT). We surveyed ICRB in consecutive Korean patients with PD who were treated with stable DRT using modified Minnesota Impulsive Disorders Interview over a period of 4 months. In the 404 patients who completed the interview and the 559 Korean healthy normal controls, genotyping was performed for variants of the DRD3 p.S9G, DRD2Taq1A, GRIN2B c.366C>G, c.2664C>T and c.-200T>G, and the promoter region of the serotonin transporter gene (5-HTTLPR). Behavioral abnormalities suggestive of ICRB including compulsive buying, gambling, sexual behavior and eating, and punding, were present in 14.4% of the patients. Variants of DRD2 and 5-HTTLPR were not associated with the risk of developing ICRB. However, the AA genotype of DRD3 p.S9G and the CC genotype of GRIN2B c.366C>G were more frequent in patients with ICRB than in nonaffected patients (odds ratio [OR] = 2.21, P = 0.0094; and 2.14, P = 0.0087, after adjusting for age and sex). After controlling for clinical variables in the multivariate analysis, carriage of either AA genotype of DRD3 or CC genotype of GRIN2B was identified as an independent risk factor for ICRB (adjusted OR: 2.57, P = 0.0087). Variants of DRD3 p.S9G and GRIN2B c.366C>G may be associated with the appearance of ICRB in PD. © 2009 Movement Disorder Society [source] | |||||||||||||||||||||||||