Schizophrenia And Disorders With Psychotic Features

Increasingly, financial reinforcement interventions based on behavioral economic principles are being applied in health care settings, and this study examined the use of financial reinforcers for enhancing adherence to medications.|Electronic databases and bibliographies of relevant references were searched, and a meta-analysis of identified trials was conducted. The variability in effect size and the impact of potential moderators (study design, duration of intervention, magnitude of reinforcement, and frequency of reinforcement) on effect size were examined.|Fifteen randomized studies and 6 nonrandomized studies examined the efficacy of financial reinforcement interventions for medication adherence. Financial reinforcers were applied for adherence to medications for tuberculosis, substance abuse, human immunodeficiency virus, hepatitis, schizophrenia, and stroke prevention. Reinforcement interventions significantly improved adherence relative to control conditions with an overall

Childhood-onset schizophrenia (COS) is a rare severe form of schizophrenia that may have greater salient genetic risk. Despite evidence for high heritability, conclusive genetic causes of schizophrenia remain elusive. Recent genomic technologies in concert with large case-control cohorts have led to several associations of highly penetrant rare copy number variants (CNVs) and schizophrenia. We previously reported two patients with COS who carried a microduplication disrupting the PXDN and MYT1L genes at 2p25.3. This rate of duplications within our COS population (N=92) is significantly higher than that in 2026 healthy controls (P=0.002). As a replication, we report a meta-analysis of four recently published studies that together provide strong evidence for an association between variably sized microduplications involving the MYT1L gene and schizophrenia. None have reported this separately. Altogether, among 5325 patients and 9279 controls, 10 microduplications were observed: nine in

Current drug treatments for schizophrenia are inadequate for many patients, and despite 5 decades of drug discovery, all of the treatments rely on the same mechanism: dopamine D(2) receptor blockade. Understanding the pathophysiology of the disorder is thus likely to be critical to the rational development of new treatments for schizophrenia.|To investigate the nature of the dopaminergic dysfunction in schizophrenia using meta-analysis of in vivo studies.|The MEDLINE, EMBASE, and PsycINFO databases were searched for studies from January 1, 1960, to July 1, 2011.|A total of 44 studies were identified that compared 618 patients with schizophrenia with 606 controls, using positron emission tomography or single-photon emission computed tomography to measure in vivo striatal dopaminergic function.|Demographic, clinical, and imaging variables were extracted from each study, and effect sizes were determined for the measures of dopaminergic function. Studies were grouped into those of

There is a well-established but poorly understood association between tobacco use and psychotic illness. The aim of this study was to determine whether tobacco use is associated with an earlier age at onset of psychotic illness.|Peer-reviewed publications in English reporting the age at onset of psychosis in tobacco-using and non-tobacco-using groups were located using searches of CINAHL, EMBASE, MEDLINE, PsycINFO and ISI Web of Science, and were supplemented by papers located by manual searches and unpublished data obtained by correspondence with primary researchers. A total of 29 samples reported age at onset data in a consecutive series of patients with a diagnosis of schizophrenia related psychosis or first episode psychosis. Information on study design, study population and effect size was extracted independently by three authors. A random effects meta-analysis was performed.|There was no significant difference between smokers and non-smokers in age at the onset of psychosis

Schizophrenia is a very complex psychiatric disorder of unknown etiology, and there is controversy as to whether its name is even appropriate to describe the associated variety of clinical presentations and symptoms. Currently, the diagnosis is essentially based on clinical criteria. These enable a clinical profile to be recognized as encompassing positive symptoms, negative symptoms, disorganization of thinking and behavior, cognitive impairment, mood abnormalities, motor abnormalities, chronic clinical course, and incomplete remissions. The concept has evolved during the past century, and schizophrenia is currently questioned as a single disease entity. Established diagnostic criteria do not mirror the heterogeneity of the disorder. A strategy to deal with clinical heterogeneity in schizophrenia is, perhaps, the adoption of a classification system based on dimensions and stages. An additional strategy to deal with etiological and pathophysiological heterogeneity is to try to

Despite the successful identification of several relevant genomic loci, the underlying molecular mechanisms of schizophrenia remain largely unclear. We developed a computational approach (NETBAG+) that allows an integrated analysis of diverse disease-related genetic data using a unified statistical framework. The application of this approach to schizophrenia-associated genetic variations, obtained using unbiased whole-genome methods, allowed us to identify several cohesive gene networks related to axon guidance, neuronal cell mobility, synaptic function and chromosomal remodeling. The genes forming the networks are highly expressed in the brain, with higher brain expression during prenatal development. The identified networks are functionally related to genes previously implicated in schizophrenia, autism and intellectual disability. A comparative analysis of copy number variants associated with autism and schizophrenia suggests that although the molecular networks implicated in these

The single-nucleotide polymorphism rs1344706, located within an intron of the ZNF804A gene, exhibits genome-wide significant association with schizophrenia. Although genotype at rs1344706 is associated with altered functional brain connectivity, the molecular mechanisms mediating its association with schizophrenia have not been clearly defined. Given its location in noncoding sequence, the authors tested association between rs1344706 and ZNF804A expression in adult and fetal human brain.|Highly quantitative measures of relative allelic expression were used to assess the effect of rs1344706 genotype on the mRNA expression of ZNF804A in the dorsolateral prefrontal cortex, hippocampus, and substantia nigra of the adult human brain and in human brain tissue from the first and second trimester of gestation.|Genotype at rs1344706 had no significant effect on the regulation of ZNF804A in any of the three adult brain regions examined. In contrast, rs1344706 genotype had a significant effect

To study the contribution of executive function to abnormal recognition of facial expressions of emotion in schizophrenia patients.|Abnormal recognition of facial expressions of emotion was assayed according to Japanese and Caucasian facial expressions of emotion (JACFEE), Wisconsin card sorting test (WCST), positive and negative symptom scale, and Hamilton anxiety and depression scale, respectively, in 88 paranoid schizophrenia patients and 75 healthy volunteers.|Patients scored higher on the Positive and Negative Symptom Scale and the Hamilton Anxiety and Depression Scales, displayed lower JACFEE recognition accuracies and poorer WCST performances. The JACFEE recognition accuracy of contempt and disgust was negatively correlated with the negative symptom scale score while the recognition accuracy of fear was positively with the positive symptom scale score and the recognition accuracy of surprise was negatively with the general psychopathology score in patients. Moreover, the WCST

To evaluate evidence for de novo etiologies in schizophrenia, we sequenced at high coverage the exomes of families recruited from two populations with distinct demographic structures and history. We sequenced a total of 795 exomes from 231 parent-proband trios enriched for sporadic schizophrenia cases, as well as 34 unaffected trios. We observed in cases an excess of de novo nonsynonymous single-nucleotide variants as well as a higher prevalence of gene-disruptive de novo mutations relative to controls. We found four genes (LAMA2, DPYD, TRRAP and VPS39) affected by recurrent de novo events within or across the two populations, which is unlikely to have occurred by chance. We show that de novo mutations affect genes with diverse functions and developmental profiles, but we also find a substantial contribution of mutations in genes with higher expression in early fetal life. Our results help define the genomic and neural architecture of schizophrenia.

NGC is the National Guideline Clearinghouse.

NGC is the National Guideline Clearinghouse.

NGC is the National Guideline Clearinghouse.