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 human small-conductance Ca(2+)-activated potassium channel gene KCNN3 has been involved in mechanisms underlying neuronal function and plasticity. A multiallelic CAG repeat polymorphism within the KCNN3 has been associated with schizophrenia and bipolar disorder. We have previously reported in a family-based study that longer CAG repeats are preferentially transmitted to patients with anorexia nervosa (AN). The present study extends the analysis of KCNN3 allele distribution to a larger series of AN female patients and control groups, incorporating information on ethnicity and co-morbidities associated with AN. The data analysis is presented while considering separately the two alleles of each individual, namely a minor (shorter) and a major (longer) allele. This study has found that the KCNN3 allele distribution in the general Israeli population does not differ significantly in at least four Jewish ethnic groups of Ashkenazi, North African, Iraqi, and Yemenite origin. These have been used as control groups in a matched case-control analysis that has demonstrated a significant over-representation of KCNN3 alleles with longer CAG repeats among AN patients (P < 0.001 for the major allele and P = 0.035 for allele sum). Under dichotomization, a significantly higher prevalence of the L allele (>19 repeats) has been observed among AN patients (P < 0.001). While considering AN and co-morbid phenotypes, a tendency towards longer (L) alleles has been observed in the subset of patients with obsessive-compulsive disorder (OCD) co-morbidity. These findings further implicate KCNN3 as a significant contributor to predisposition to AN.
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PMID:CAG repeat polymorphism within the KCNN3 gene is a significant contributor to susceptibility to anorexia nervosa: a case-control study of female patients and several ethnic groups in the Israeli Jewish population. 1538 73

The study examined the ethnic ratio of 16 DSM-III mental disorders among White, Black, Hispanic, and Asian Americans. A total of 18,126 residents from 5 sites and 2,939 residents from the Epidemiological Catchment Area's Los Angeles site were studied separately. Logistic regression analysis was performed. Results showed that Blacks were significantly less likely than Whites to have major depressive episode, major depression, dysthymia, obsessive-compulsive disorder, drug and alcohol abuse or dependence, antisocial personality, and anorexia nervosa, but they were significantly more likely than Whites to have phobia and somatization. Lifetime prevalence rates of schizophrenia, obsessive-compulsive disorder, panic, and drug abuse or dependence were significantly lower among Hispanics than among Whites. Asians also had significantly lower rates than Whites of schizophreniform, manic episode, bipolar disorder, panic, somatization, drug and alcohol abuse or dependence, and antisocial personality. Compared with the overall findings, ethnic differences at the Los Angeles site were lessened between Blacks and Whites, enhanced between Hispanics and Whites, and basically unchanged between Asians and Whites.
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PMID:Ethnic characteristics of mental disorders in five U.S. communities. 1560 83

Altered motor activity is a frequently observed symptom in many psychiatric disorders. It is an important diagnostic parameter in mania, depression, ADHD and others. The method which allows measuring motor activity precisely and objectively is actometry. An actometer is a small, electronic device measuring body movements. This paper is a review of psychiatric research in which actometry was used: sleep disorders, ADHD, schizophrenia, anorexia nervosa, affective disorders and also in chronobiology and psychopharmacology. Methodology of actometric research and limitations of the method are discussed.
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PMID:[Application of actigraphy in psychiatry]. 1577 76

This report summarizes the background and specific objectives for a symposium on the neurobiology of nonhomeostatic eating and drug abuse that was held at the 2004 Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB). The symposium was the first of a series funded by a conference grant from four institutes of the National Institutes of Health. The encompassing goal of the series is to analyze the roles for the biological mechanisms of ingestion in obesity, eating disorders and other theoretically related areas including addiction, depression and schizophrenia. The symptoms and treatments of these diverse pathologies routinely involve aberrations in the mechanisms regulating eating and body weight. The presentations and discussion from this symposium (1) identified changes in neurotransmitter dynamics and gene expression in brain "reward circuits" accompanying learning of behaviors to obtain palatable foods or drugs of abuse; (2) analyzed behavioral findings in animals and humans, and neuroimaging data in humans, supporting treatment with GABA(B) agonists to reduce craving for drugs of abuse and possibly for highly rewarding foods; and (3) used neuroimaging data in humans to establish novel serotonergic targets for normalizing reward processes and impulse control in anorexia nervosa and bulimia. Overall, the symposium clearly revealed our rapidly broadening understanding of the alterations in the brain at the molecular, cellular and systems levels that are associated with craving and nonhomeostatic consumption of food and drugs of abuse. This knowledge gained largely in animal models translates to novel and better strategies for treating human patients.
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PMID:NIH symposium series: ingestive mechanisms in obesity, substance abuse and mental disorders. 1612 61

Since identification of the genetic component in anorexia nervosa (AN), genes that partake in serotonergic and dopaminergic systems and in hormonal and weight regulation have been suggested as potential candidates for AN susceptibility. We propose another set of candidate genes. Those are genes that are involved in the signaling pathway using NMDA-R and SK channels and have been suggested as possible effectors of NMDA-R driven signaling. The role of NMDA-R in the etiology of schizophrenia has already been substantiated on various levels. Several studies based on population and family groups have implicated SK3 in schizophrenia and more recently in AN as well. Our study group consisted of 90 AN family trios. We examined the transmission of two potentially functional polymorphisms, 5073T>G polymorphism in the gene encoding the NR2B subunit of NMDA-R and CAG repeats in the coding region of SK3 channel gene. Using HHRR and TDT approaches, we found that both polymorphisms were preferentially transmitted to AN offspring (TDT yielded chi(2)=5.01, p=0.025 for NR2B 5073G alleles and chi(2)=11.75, p<0.001 for SK3 L alleles including >19 repeats). Distribution analysis of the combined NR2B/SK3 genotypes suggests that the contribution of both polymorphisms to AN risk is independent and cumulative (OR=2.44 for NR2B GG genotype and OR=3.01 for SK3 SL and LL genotypes, and OR=6.8 for the combined NR2B/SK3 genotypes including high-risk alleles). These findings point to the contribution of genes associated with the NMDA-R signaling pathway to predisposition and development of AN.
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PMID:Dual contribution of NR2B subunit of NMDA receptor and SK3 Ca(2+)-activated K+ channel to genetic predisposition to anorexia nervosa. 1615 52

The aim of the study was to investigate the extent of social anxiety in different mental disorders. A total of 341 patients aged 7-18 years participated in the study. To measure social anxiety, the German version (SPAIK) of the Social Phobia and Anxiety Inventory for Children (SPAI-C) was used. Subgroups were built dependent on mental disorders. A total score above 20, which was assumed to indicate social anxiety, was observed in children with selective mutism (n = 9; M = 22.68; SD = 11.29) and in children with Asperger's Syndrome (n = 7; M = 20.77; SD = 13.77). Patients who had the following mental disorders also showed a higher total score of social anxiety: obsessive-compulsive disorder, anorexia nervosa, schizophrenia, depression and conduct disorder. In none of these disorders, however, did the mean total score exceed the cut-off of 20.
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PMID:The extent of social anxiety in combination with mental disorders. 1652 52

124 girls with anorexia nervosa were investigated. Two types of anorexia nervosa course were revealed. The disease takes its benign course, without derangement of social adaptation in patients having strain of hysteria; those with schizoid stigmas have food reaction abnormality as a debut of schizophrenia.
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PMID:[Anorexia nervosa variants and their correction]. 1705 14

The link between degree of urbanisation and a number of mental disorders is well established. Schizophrenia, psychosis and depression are known to occur more frequently in urban areas. In our primary care-based study of eating disorders, the incidence of bulimia nervosa showed a dose-response relation with degree of urbanisation and was five times higher in cities than in rural areas. Remarkably, anorexia nervosa showed no association with urbanisation. We conclude that urban life is a potential environmental risk factor for bulimia nervosa but not for anorexia nervosa. These findings provide a promising avenue for further research into the aetiology of eating disorders.
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PMID:Urbanisation and the incidence of eating disorders. 1713 44

The aim of this study was to assess dose-related steady-state serum concentrations of olanzapine (OLZ) and its metabolites N-desmethyl OLZ (DMO) and 2-hydroxymethyl OLZ (2-OH-OLZ) (assessed by high-performance liquid chromatography) in 122 child and adolescent psychiatric patients (age 16.9 +/- 2.2, range, 10-21 years; 74 males, 48 females) with a variety of diagnoses: schizophrenia group (n = 80); nonschizophrenia group (n = 29); anorexia nervosa (AN) group (n = 13). Median OLZ serum concentrations were 32.7 (range, 1-118; all patients), 37.7 (2-115; schizophrenia group), and 18.7 (1-63, AN group) ng/mL. The median OLZ concentration-to-dose (C/D) ratio (n = 122) was 2.6, with 90% of the distribution between 0.8 and 5.5 (ng/mL)/(mg/d). OLZ concentration was significantly correlated with DMO (r = 0.567; P < 0.0005) but not with 2-OH-OLZ (r = 0.122; P = 0.188). Daily OLZ dose was correlated with OLZ concentration in all (r = 0.684; P < 0.0005), schizophrenic (r = 0.542; P < 0.0005), and AN (r = 0.805; P = 0.001) patients, respectively. Patients aged less than 16 years displayed similar C/D for OLZ (P = 0.58) but higher C/D for DMO (P = 0.003) than those 16 years or older. AN patients received lower median OLZ doses (7.5; 5-15 mg) than schizophrenic patients (12.5; 2.5-40 mg), even after correcting for body mass index (P = 0.02). OLZ dose did not differ (P = 0.088) between smokers and nonsmokers, but smokers showed lower C/D for OLZ than nonsmokers (P = 0.008). C/D for OLZ was 38% higher (P = 0.041) under comedication with selective serotonin reuptake inhibitors when compared with OLZ monotherapy. Multiple linear regression analysis revealed that 46% of the variation of OLZ concentration can be explained by dose, diagnosis, age, sex, smoking, and comedication. The data are compared with the literature, and the relevance of therapeutic antipsychotic drug monitoring in previously sparsely investigated subgroups, such as children and adolescents or patients with AN, is emphasized.
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PMID:Serum levels of olanzapine and its N-desmethyl and 2-hydroxymethyl metabolites in child and adolescent psychiatric disorders: effects of dose, diagnosis, age, sex, smoking, and comedication. 1716 90

Anorexia nervosa is a rare psychiatric disorder and epidemiological studies have shown a female to male ratio of 10:1, suggesting it is a disorder predominantly seen among females. The prevalence of anorexia nervosa comorbid with other psychiatric disorders has been reported to be quite high. Whereas depression and anxiety disorders are the most common comorbid diagnoses in anorexic patients, the dual-diagnosis of anorexia and schizophrenia is a relatively rare condition. Based generally on the observations from single case reports or case series, several explanations have been made about the co-occurrence of anorexia and schizophrenia. Herein, we present a male patient who developed schizophrenia after an anorexic period of 4 years that began when he was 14 years old with the decision to lose weight, which then progressed to a pattern of disordered eating and body image. This case is rare because the patient is male and has a comorbid diagnosis of anorexia nervosa and schizophrenia. To the best of our knowledge, there is only one previous case report in the literature describing a male anorexic patient with comorbid schizophrenia. In this case presentation, the diagnosis of anorexia nervosa in males is addressed, the definition and significance of sub-threshold cases are discussed, and the comorbidity of anorexia nervosa and schizophrenia are reviewed in light of the literature.
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PMID:[Case report: comorbid anorexia nervosa and schizophrenia in a male patient]. 1736 72


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