Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The data reviewed confirm that mentally ill patients smoke twice as many cigarettes as patients without mental illness. The secretion of neurotransmitters such as noradrenaline, serotonin, dopamine, acetylcholine, gamma-amino-butyric acid and glutamate is increased by the binding of nicotine to central nicotine receptors. There are also data showing that serotonin formation and secretion in patients with mental illness are influenced by chronic smoking. Cigarette smoke inhibits the activity of monoamine oxidase B, which is responsible for the catabolism of several brain neurotransmitters. Patients suffering from major depression show a comorbidity between heavy smoking and the disease. In patients with schizophrenia treated with neuroleptics, increased cigarette smoking reduces adverse reactions to the drug therapy presumably because of an increase in metabolism of the neuroleptics. There is also evidence suggesting that quitting smoking is more difficult for mentally ill patients than patients without psychiatric disease. Several studies have been carried out on smoking cessation in psychiatric patients. The alternative method of harm reduction, e.g. reducing the number of cigarettes smoked using nicotine patches or chewing gum, is necessary in patients not able to quit. The data indicate that strategies such as the coupling of smoking prohibition with administration of nicotine preparations are useful in smoking cessation. A no-smoking policy in psychiatric clinics, even when this leads to withdrawal symptoms in the patients affected, has no negative effect on mental illness. Because patients with mental diseases are particularly vulnerable to the marketing strategies of the tobacco industry, this chronically ill section of the population requires special protection by the law-makers.
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PMID:A review of the pharmacological and psychopharmacological aspects of smoking and smoking cessation in psychiatric patients. 1235 57

Several lines of evidence suggest that tardive dyskinesia (TD) may be associated with altered dopaminergic neurotransmission. We hypothesized that deranged dopamine degradation enzyme activities might be related to the susceptibility to TD through altered dopaminergic neurotransmission in the central nervous system. In the present study, we investigated the relationship between the gene polymorphisms of three dopamine degradation enzymes and TD. We genotyped the valine/methionine polymorphism of codon 108/158 in the catechol-O-methyltransferase (COMT) gene, the 30-bp repeat polymorphism in the promoter of the monoamine oxidase A (MAOA) gene, and the A/G polymorphism in intron 13 of the monoamine oxidase B (MAOB) gene in 206 Japanese patients with schizophrenia. No significant difference was found in total scores on the Abnormal Involuntary Movement Scale (AIMS) among the subject groups, sorted according to the COMT, MAOA and MAOB genotypes. Moreover, no significant difference was found in allele frequencies between patients with TD and patients without TD for any of the polymorphisms. As both COMT and MAO genes are involved in degrading catecholamines, we also sought evidence for additive and epistatic effects, but none was observed. Our data, therefore, do not support the hypothesis that polymorphisms in COMT, MAOA, and MAOB genes are involved individually or in combination in the predisposition to TD.
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PMID:Polymorphisms of dopamine degradation enzyme (COMT and MAO) genes and tardive dyskinesia in patients with schizophrenia. 1526 99

Amin oxydase (monoaminoxydase, MAO) is an enzyme which catalyses chemical reactions of biogenic amines. It plays a crucial role in pathogenesis of mental disorders associated with the dysfunction of the central monoaminergic systems (schizophrenia, affective disorders, some forms of alcohol dependence, and personality disorders). MAO has got two isoforms such as MAO-A and MAO-B. The genes coding of MAO are localised at the short arm of chromosome Xp11. In each sequence of genes there is a probability of functional polymorphism occurrence which leads to a variable expression or a change of MAO activity and it exerts an impact on the onset of some mental disorders, such as: schizophrenia, affective disorders, some forms of alcohol dependence, and personality and behavioural disorders. Dynamic development of psychiatric genetics may have crucial impact on considerable progress in understanding molecular background of mental disorders.
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PMID:[Genetic polymorphism of a MAO in mental disorders]. 1804 79

The ancestral susceptibility hypothesis has been proposed to explain the existence of susceptibility alleles to common diseases. Some ancestral alleles, reflecting ancient adaptations, may be poorly adapted to the more contemporary environmental conditions giving rise to an increased risk to suffer some common disorders. In order to test this hypothesis in schizophrenia, we focused on the monoamine oxidase B gene (MAOB). This gene is involved in deamination of several monoamines, including both xenobiotic amines present in several foods, as well as neurotransmitters such as dopamine. In addition, preliminary analysis based on phase I HapMap data suggested that recent natural selection has acted on this locus. We further explored the existence of this recent positive selection using a test based on extension of linkage disequilibrium (LD) to large distance at the specific selected haplotype taking data from HapMap phase II, and searched for association of the ancestral haplotypes with schizophrenia in a sample of 532 schizophrenic patients and 597 controls from Spain. Our analysis suggested the existence of a haplotype of MAOB subject to recent selection. In agreement with the ancestral susceptibility hypothesis, the ancestral haplotypes were significantly over-represented in patients (P = 0.047). These haplotypes conferred an increased risk to schizophrenia, restricted to males (P = 0.024, OR = 1.41, 95% CI 1.01-1.90). Thus, pending on replication studies, MAOB seems to fit the ancestral susceptibility model, validating a new strategy to search for common schizophrenia susceptibility genes by focusing in those functional candidate genes subject to recent positive selection.
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PMID:Recent adaptive selection at MAOB and ancestral susceptibility to schizophrenia. 1855 63

We tested four genes [phenylalanine hydroxylase (PAH), the serotonin transporter (SLC6A4), monoamine oxidase B (MAOB), and the gamma-aminobutyric acid A receptor beta-3 subunit (GABRB3)] for their impact on five schizophrenia symptom factors: delusions, hallucinations, mania, depression, and negative symptoms. In a 90 family subset of the Irish Study of High Density Schizophrenia Families, the PAH 232 bp microsatellite allele demonstrated significant association with the delusions factor using both QTDT (F=8.0, p=.031) and QPDTPHASE (chi-square=12.54, p=.028). Also, a significant association between the GABRB3 191 bp allele and the hallucinations factor was detected using QPDTPHASE (chi-square=15.51, p=.030), but not QTDT (chi-square=2.07, p=.560).
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PMID:Polymorphisms in SLC6A4, PAH, GABRB3, and MAOB and modification of psychotic disorder features. 1926 43

We present a schizophrenia association study using an extensive linkage disequilibrium (LD) mapping approach in seven candidate genes with a well established link to dopamine, including receptors (DRD2, DRD3) and genes involved in its metabolism and transport (ACE, COMT, DAT, MAO-A, MAO-B). The sample included 242 subjects diagnosed with schizophrenia and related disorders and 373 hospital-based controls. 84 tag SNPs in candidate genes were genotyped. After extensive data cleaning 70 SNPs were analyzed for association of single markers and haplotypes. One block of four SNPs (rs165849, rs2518823, rs887199 and rs2239395) in the 3' downstream region of the COMT gene which included a non-dopaminergic candidate gene, the ARVCF (Armadillo like VeloCardio Facial) gene, was associated with the risk of schizophrenia. The genetic region including the ARVCF gene in the 22q11.21 chromosome is associated with schizophrenia in a Spanish series. Our results will assist in the interpretation of the controversy generated by genetic associations of COMT and schizophrenia, which could be the result of different LD patterns between COMT markers and the 3' region of the ARVCF gene.
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PMID:ARVCF single marker and haplotypic association with schizophrenia. 1950 83

Two X-linked microsatellites, (AC)n repeats at the monoamine oxidase (MAO) A locus and (TG)n repeats at the MAO-B locus, were typed by using a PCR-based procedure in 89 nuclear families consisting of mothers, fathers and female affected offspring with schizophrenia or mothers and male affected offspring. A haplotype-based haplotype relative risk (HHRR) approach was applied to detect allelic association of these two microsatellites with schizophrenia. In the families of male patients, a significant difference in frequency distribution was found between transmitted and non-transmitted (TG)n repeats (chi(2) = 15.13, df = 6, P = 0.019), and Fisher's exact test showed that allelic frequency of the transmitted (TG)(24) was significantly higher than that of the non-transmitted (TG)(24) (Fisher's P = 0.003). However, no significant differences in frequency distribution between mother- or father-transmitted and non-transmitted (TG)n repeats were found in the families of female patients. No significant differences in frequency distribution were found between transmitted and non-transmitted (AC)n repeats in the families of either male patients or female patients. The present study suggests that the MAO-B gene may be associated with schizophrenia, and the underlying genetic mechanism of schizophrenia may differ between male and female schizophrenic individuals.
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PMID:Allelic association between dinucleotide repeats at the monoamine oxidase loci and schizophrenia. 1969 56

Autism spectrum disorder (ASD) and schizophrenia (SCZ) are two common neurodevelopmental syndromes that result from the combined effects of environmental and genetic factors. We set out to test the hypothesis that rare variants in many different genes, including de novo variants, could predispose to these conditions in a fraction of cases. In addition, for both disorders, males are either more significantly or more severely affected than females, which may be explained in part by X-linked genetic factors. Therefore, we directly sequenced 111 X-linked synaptic genes in individuals with ASD (n = 142; 122 males and 20 females) or SCZ (n = 143; 95 males and 48 females). We identified >200 non-synonymous variants, with an excess of rare damaging variants, which suggest the presence of disease-causing mutations. Truncating mutations in genes encoding the calcium-related protein IL1RAPL1 (already described in Piton et al. Hum Mol Genet 2008) and the monoamine degradation enzyme monoamine oxidase B were found in ASD and SCZ, respectively. Moreover, several promising non-synonymous rare variants were identified in genes encoding proteins involved in regulation of neurite outgrowth and other various synaptic functions (MECP2, TM4SF2/TSPAN7, PPP1R3F, PSMD10, MCF2, SLITRK2, GPRASP2, and OPHN1).
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PMID:Systematic resequencing of X-chromosome synaptic genes in autism spectrum disorder and schizophrenia. 2047 60

The monoamine systems have been suggested to play a role in the biological basis of attention-deficit hyperactivity disorder (ADHD) symptoms. Thus, polymorphisms, for example, in the monoamine oxidase A (MAOA) and the serotonin transporter (5HTT) genes have been associated with ADHD-like phenotypes. Furthermore, platelet monoamine oxidase B (MAOB) activity has frequently been linked to impulsiveness-related traits. In this study, we have studied ADHD symptoms with regard to the combination of platelet MAOB activity and MAOA-variable number of tandem repeats (VNTR) or 5HTT-LPR genotype. The study group consisted of 156 adolescent twin pairs, that is, 312 individuals, who participated in a previous study. ADHD symptoms were scored with a structured clinical interview of both the twins and a parent using Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version. The presence of a short 5HTT-LPR or short MAOA-VNTR allele, in combination with high levels of platelet MAOB enzyme activity was associated with higher scores of ADHD-like problems (P<0.001 and 0.01, respectively). This re-examination of ADHD scores in a nonclinical sample suggests that effects of MAOA-VNTR and 5HTT-LPR are moderated by platelet MAOB activity.
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PMID:Associations of MAOA-VNTR or 5HTT-LPR alleles with attention-deficit hyperactivity disorder symptoms are moderated by platelet monoamine oxidase B activity. 2161 May 56

To check experimentally the hypothesis of schizophrenia being a manifestation of extremely low threshold of hypnotic (catatonic) type of reaction, changes of some neurophysiologic and neurochemical systems in rats with a genetic predisposition to catalepsy were compared to analogous changes found so far in schizophrenia or chronic amphetamine intoxication considered nowadays as the most adequate pharmacological model of schizophrenia. It is found that in rats predisposed to catalepsy the threshold of audiogenic seizures is elevated; the activity of tryptophan hydroxylase in striatum is higher in rats predisposed to catalepsy genetically and due to a chronic methylphenidate intoxication as compared to control animals; noradrenaline content and noradrenaline/dopamine ratio is lower in the diencephalon of rats predisposed to catalepsy than in controls; cataleptic rats have a higher content of homovanillic acid in N.accumbens , and a higher frequency of inversion of hemispheric asymmetry as estimated by levels of dopamine and dioxyphenylacetic acid in N.accumbens and caudate nucleus, than normal rats; MAO-B/MAO-A ratio is higher in the brain stem of cataleptic than normal rats. The effects of haloperidol and apomorphine on motor activity of cataleptic and normal animals point to a higher sensitivity of postsynaptic dopamine receptors in the former. Conditioned avoidance reaction is formed slower, but preserved longer in rats predisposed to catalepsy. Blood serum of wild rats predisposed to akinetic catatonic reactions, unlike the serum of normal wild rats, inhibits the electric activity of snail neurons. The above indicated changes are analogous to those known to be present in schizophrenia and/or chronic intoxication with amphetamine or its pharmacological analogues, which witnesses in favour of the proposed hypothesis.
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PMID:Experimental studies on genetically determined predisposition to catatonia in rats as a model of schizophrenia. 2492 95


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