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)

Microdeletion 22q11.2 (22q11DS) is the most frequent chromosomal deletion known in man. Velocardiofacial syndrome is one of numerous clinical syndromes that can be attributed to this micro deletion. There is an increasing recognition of associations with neuropsychiatric disorders. Particularly, schizophrenic psychosis, attention-deficit/hyperactivity disorder (ADHD), intellectual impairment and learning disabilities, seizures and motoric abnormalities have been identified in patients with 22q11DS. Recent studies supported the association of schizophrenia and 22q11DS, but the pathogenetic implications for idiopathic schizophrenia are still controversial. We report on two clinical cases in which psychotic symptoms led to the molecularcytogenetic diagnosis of microdeletion 22q11.2. Additionally, this article gives a systematic review of literature regarding psychiatric disorders, neurologic symptoms and partly corresponding morphological brain abnormalities in 22q11 deletion syndromes.
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PMID:[Spectrum of neuropsychiatric features associated with velocardiofacial syndrome (Deletion 22q11.2)]. 1675 38

There is little research on characteristics related to course and prognosis of early-onset psychosis. The present article aims to advance our knowledge of this disorder for the purpose of proper diagnosis and treatment. It focuses on premorbid and prodromal characteristics, treatment history, symptoms and classifications, and differences between subgroups with affective and schizophrenic psychosis. A chart review was constructed to study a group of 129 subjects (12-18 years) with psychotic symptoms referred to the University Medical Center in Utrecht. The group was characterized by early-but nonspecific-treatment, developmental problems (mostly social), and clear prodromal symptoms. Drug abuse, depressive symptoms, and suicidal behavior were also frequent. Male sex, a relatively long prodromal phase, school problems, and drug abuse were more indicative of the schizophrenic subgroup. Introversion was characteristic for boys with schizophrenia. Classifications, however, were not stable. These findings suggest that early recognition of psychosis can be enhanced in health and youth care facilities. Careful examination of the prodromal phase seems helpful to differentiate between schizophrenic and affective psychosis.
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PMID:Characteristics of early psychosis. 1706 66

This case presentation involves a family study looking at the inheritance of schizophrenic psychosis. It refers to the increasing risk of disease in correlation to the closeness of the relationship. The study includes both affected parents, their three children and one grandchild, all of whom had multiple hospital admissions and received psychiatric treatment. The clinical features were typical of schizophrenia. The severity of illness increased within the later generation. This study indicates a high risk correlation in this family and is in keeping with other current field studies.
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PMID:[Contribution to the inheritance of schizophrenic psychosis]. 1719 14

Leuproreline acetate is a gonadotropin-releasing hormone (GnRH) analog which is used for in vitro fertilization (IVF) treatment. This compound suppresses gonadal estrogen secretion prior to hormonal stimulation. We report a 37-year-old woman who suffered from a schizoaffective psychosis for several years. She received IVF treatment with leuproreline acetate (Uno-Enantone) because of primary infertility. Under this treatment she developed acute schizoaffective symptoms. Suppression of gonadal secretion can result in exacerbation of schizophrenic psychosis, which is in line with the hypothesis of protective effects of estrogen in schizophrenia. We recommend that IVF treatment with leuproreline acetate in patients with psychiatric disorders be initiated only with special attention to their mental condition. In addition, patients should be informed about the possible mental effects of the treatment.
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PMID:[Exacerbation of a schizoaffective psychosis after in vitro fertilization with leuproreline acetate]. 1748 67

Reduced amplitudes of auditory evoked mismatch negativity (MMN) have often been found in schizophrenic patients, indicating deficient auditory information processing and working memory. Cannabis-induced psychotic states may resemble schizophrenia. Currently, there are discussions focusing on the close relationship between cannabis, the endocannabinoid and dopaminergic system, and the onset of schizophrenic psychosis. This study investigated the effects of cannabis on MMN amplitude in 22 healthy volunteers (age 28+/-6 years, 11 male) by comparing Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and standardized cannabis extract containing Delta(9)-THC and cannabidiol (CBD) in a prospective, double-blind, placebo-controlled cross-over design. The MMNs resulting from 1000 auditory stimuli were recorded by 32 channel EEG. The standard stimuli were 1000 Hz, 80 dB SPL, and 100 ms duration. The deviant stimuli differed in frequency (1500 Hz). Significantly greater MMN amplitude values at central electrodes were found under cannabis extract, but not under Delta(9)-THC. There were no significant differences between MMN amplitudes at frontal electrodes. MMN amplitudes at central electrodes were significantly correlated with 11-OH-THC concentration, the most important psychoactive metabolite of Delta(9)-THC. Since the main difference between Delta(9)-THC and standardized cannabis extract is CBD, which seems to have neuroprotective and anti-psychotic properties, it can be speculated whether the greater MMN amplitude that may imply higher cortical activation and cognitive performance is related to the positive effects of CBD. This effect may be relevant for auditory cortex activity in particular because only MMN amplitudes at the central, but not at the frontal electrodes were enhanced under cannabis.
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PMID:Acute effects of Delta9-tetrahydrocannabinol and standardized cannabis extract on the auditory evoked mismatch negativity. 1788 51

Serotonin (5-HT) has been implicated in the pathophysiology of several psychiatric disorders including major depressive disorder (MDD) and schizophrenia (SCZ). The serotonin transporter (5-HTT) is a major regulator of 5-HT function. 5-HTT gene polymorphic variants have been associated with both MDD and SCZ. A case-control design was used for candidate gene-disease association in 194 MDD patients, 155 schizophrenic psychosis patients, and 246 healthy controls, all North European Caucasians. Four polymorphisms were analyzed in terms of genotype, allele, and haplotype-based associations. Linkage disequilibrium (LD) analysis was also carried out. Bonferroni correction was used for multiple testing. Haplotype-based analyses showed significant associations between 5-HTT and SCZ but not MDD. No single locus associations were observed. In agreement with published meta-analysis our results indicate that 5-HTT associates with SCZ but not with MDD. It appears that risk for SCZ maps within a specific 5-HTT haplotype block.
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PMID:Haplotype analysis confirms association of the serotonin transporter (5-HTT) gene with schizophrenia but not with major depression. 1788 57

Neurophysiological methods allow the examination of cognitive-cortical functioning in patients with schizophrenia in its prodromal states. As revealed by previous studies, event-related potential components such as auditory evoked P300 associated with cognitive processes, such as attention and orientation, are known to be reduced in amplitude in acute and chronic as well as in medicated and unmedicated patients. It is, however, unclear whether a P300 amplitude reduction occurs before the schizophrenic psychosis is fully manifested. We studied patients in the prodromal phase of the schizophrenic disorder (i.e. subjects with an at-risk mental state showing attenuated psychotic symptoms or brief limited intermittent symptoms) as well as first-episode patients and chronic patients with schizophrenia and compared these groups to healthy subjects. The event-related P300 was recorded during an auditory oddball paradigm. Groups differed significantly from each other in the P300 amplitude at Pz (F(3/149)=2.532, p=0.02). Post-hoc tests revealed significantly lower P300 amplitudes of non-medicated prodromal (p=.03), first-episode (p=.01) and chronic patients (p=.001) compared to the healthy controls. The study revealed that there are neurophysiological changes as the reduction in P300 amplitudes begins early in schizophrenia at the prodromal phase, i.e. before a manifestation of full-blown psychosis, and that these changes seem to have a progressive course from prodromal to chronic state of schizophrenia as assumed in this cross-sectional study.
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PMID:Reduction of auditory event-related P300 amplitude in subjects with at-risk mental state for schizophrenia. 1862 46

Since Kraepelin called dementia praecox what we nowadays call schizophrenia, cognitive dysfunction has been regarded as central to its psychopathological profile. Disturbed experience and integration of emotions are, both intuitively and experimentally, likely to be intermediates between basic, non-social cognitive disturbances and functional outcome in schizophrenia. While a number of studies have consistently proven that, as part of social cognition, recognition of emotional faces and voices is disturbed in schizophrenics, studies on multisensory integration of facial and vocal affect are rare. We investigated audiovisual integration of emotional faces and voices in three groups: schizophrenic patients, non-schizophrenic psychosis patients and mentally healthy controls, all diagnosed by means of the Schedules of Clinical Assessment in Neuropsychiatry (SCAN 2.1). We found diminished crossmodal influence of emotional faces on emotional voice categorization in schizophrenics, but not in non-schizophrenia psychosis patients. Results are discussed in the perspective of recent theories on multisensory integration.
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PMID:Audiovisual emotion recognition in schizophrenia: reduced integration of facial and vocal affect. 1898 99

Glutamatergic neurotransmission is critically involved into the pathogenesis of schizophrenic psychosis, in particular regarding cognitive and negative symptoms. The reported molecular mechanisms include increased glutamate transporter expression and antipsychotic agents such as clozapine were found able to suppress the expression of these genes. So far, the effects of the partial dopaminergic and serotonergic agonist aripiprazole on glutamatergic neurotransmission were never investigated. In a rat animal model of long-term antipsychotic treatment, we analyzed the expression of glutamate transporter genes after treatment with aripiprazole. Groups of 6 male Sprague-Dawley rats were treated for 4 weeks or 4 months with daily oral doses of 10 or 40mg aripiprazole per kg. Using semi-quantitative in situ-hybridization, we assessed the expression of pre- and post-synaptic glutamate transporter genes. Compared to control animals, differential expression levels were found in several cortical and hippocampal regions. The astroglial excitatory amino acid transporter genes EAAT1 and EAAT2 as well as the neuronal transporter EAAT3 were suppressed, while the presynaptic vesicular glutamate transporter vGluT1 was transiently induced in hippocampal subregions and EAAT4 was transiently suppressed in frontocortical areas. These transcriptional effects exerted by aripiprazole may counteract a glutamatergic deficit state and strengthen the neurotransmission of glutamate with positive consequences on cognitive and negative symptoms of schizophrenia.
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PMID:Differential expression of glutamate transporter genes after chronic oral treatment with aripiprazole in rats. 1952 31

A dysregulation of the mesolimbic dopamine system in schizophrenia patients may lead to aberrant attribution of incentive salience and contribute to the emergence of psychopathological symptoms like delusions. The dopaminergic signal has been conceptualized to represent a prediction error that indicates the difference between received and predicted reward. The incentive salience hypothesis states that dopamine mediates the attribution of "incentive salience" to conditioned cues that predict reward. This hypothesis was initially applied in the context of drug addiction and then transferred to schizophrenic psychosis. It was hypothesized that increased firing (chaotic or stress associated) of dopaminergic neurons in the striatum of schizophrenia patients attributes incentive salience to otherwise irrelevant stimuli. Here, we review recent neuroimaging studies directly addressing this hypothesis. They suggest that neuronal functions associated with dopaminergic signaling, such as the attribution of salience to reward-predicting stimuli and the computation of prediction errors, are indeed altered in schizophrenia patients and that this impairment appears to contribute to delusion formation.
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PMID:Dopaminergic dysfunction in schizophrenia: salience attribution revisited. 2040 23


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