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)

A common polymorphism in the alpha1-antichymotrypsin (ACT) gene is associated with Alzheimer's disease. ACT is also a trophic factor in the hippocampal neurons. In order to examine if the ACT gene plays a role in the pathogenesis of schizophrenic disorders, patients (n = 175) and control subjects (n = 114) were genotyped for ACT. We also investigated the relationship between genotypes and patients' cognitive function as evaluated by the Clinical Dementia Rating Scale and the Mini-Mental State Examination. The results demonstrated no association between schizophrenia and/or cognitive deficit in schizophrenia and ACT polymorphism. The data suggest that the ACT gene is not of major importance for the genesis of schizophrenia. Further studies measuring ACT expression as messenger RNA or serum ACT level may help to exclude the role of ACT in the pathogenesis of schizophrenia.
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PMID:Alpha-1-antichymotrypsin polymorphism in schizophrenia: frequency, age at onset and cognitive function. 1047 60

Signal detection theory is appropriate for analyzing the problem of whether auditory hallucination arises from a sensory or judgmental disorder. In the present study the sensory discrimination ability and decision bias of psychiatric patients with auditory hallucination was investigated by using the visual continuous performance test. Based on signal detection theory the d' (d prime) and the lnbeta value (the natural logarithm of the beta value) were calculated. The d' is indicator of discriminating ability, whereas the lnbeta value is an indicator of decision bias. The psychiatric inpatients with the diagnosis of schizophrenia mainly were divided into 11 patients with auditory hallucinations (AH(+)) and 11 patients without hallucinations (AH(-)). As compared with the AH(-) group, the AH(+) group showed the same d' value and a significantly lower lnbeta value. As compared with the normal control group, the AH(+) group showed a significantly lower d' value and a nearly normal lnbeta value. These results suggest that auditory hallucination is characterized by a cognitive deficit of unreasonably maintaining a relatively risk-taking decision bias in spite of decreased discriminating ability, which opposes the interpretation of Bentall and Slade (1985). The AH(+) group was divided into subgroups with bizarre delusions (BD(+)) and without bizarre delusions (BD(-)). The BD(+) group showed a stronger tendency toward a lower d' value and normal lnbeta value, which the AH(+) group had.
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PMID:The signal detection ability of patients with auditory hallucination: analysis using the continuous performance test. 1049 28

Among the reasons for the relatively limited number of investigations of self-knowledge phenomena should be included, in addition to theoretical motives, the difficulties regarding the use of instruments available for this kind of approach and their content validity. This study investigates the relationship between subjective and objective deficits in schizophrenia, taking into account subjective experiences of cognitive impairment, clinical symptoms, and cognitive evoked potentials (P300 component). A group of 36 young schizophrenic patients (29 on neuroleptic treatment and seven drug-naive) were considered, together with a comparison group of 36 healthy subjects. Auditory event-correlated potentials (ERPs) were obtained using a simple "oddball" paradigm. Clinical symptoms were rated with the Brief Psychiatric Rating Scale (BPRS) and Scales for the Assessment of Positive and Negative Symptoms (SAPS and SANS), and while subjective disturbances were assessed by the Frankfurter Beschwerde Fragebogen (FBF, also called the Complaint Questionnaire). Correlation analysis showed that P300 amplitude was inversely correlated with subjective experiences of cognitive deficit, especially in the area of automatic skills and overstimulation. No relationship emerged between BPRS, SANS, and SAPS scores and P300 alterations. The results suggest that subjective cognitive disturbances, more than objective symptoms, are related to P300 alterations in schizophrenia, and that the FBF questionnaire appropriately covers the domain of schizophrenic cognitive disorders.
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PMID:Basic symptoms and P300 abnormalities in young schizophrenic patients. 1050 19

'Working memory' dysfunction has been proposed as a central cognitive feature in schizophrenia. To further explore this issue we developed a computerized easy and fast to administer test using the standard keyboard as visual-manual subject-computer interface along a delayed-response paradigm. The test has been administered to 25 patients who met the DSM-III-R criteria for schizophrenia and 25 healthy control subjects matched as possible for sex. The data confirm the visuo-spatial 'working memory' dysfunction in schizophrenic patients. The test maintains the discriminative capacity of similar previously devised tasks with the advantages of being usable on almost every standard computer and shorter and more acceptable for severely disabled patients also. The test can be considered an useful tool to study the 'working memory' impairment in the cognitive deficit of schizophrenia.
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PMID:Spatial working memory assessment by a visual-manual delayed response task: a controlled study in schizophrenia. 1055 72

Performance of participants diagnosed with schizophrenia on the Sentence Arrangement subtest of the WAIS-R NI and several tests sensitive to frontal lobe dysfunction was significantly poorer than that of manic depressive or control participants. Several measures of performance of patients diagnosed with schizophrenia on the WAIS-R NI Sentence Arrangement subtest appeared to support recent interpretations of the cognitive deficit seen in schizophrenia. These data represent the first demonstration of deficit performance by patients with schizophrenia on the Sentence Arrangement subtest. This is also supportive of the prediction that one of the areas whose activity may influence scores on this subtest is the prefrontal cortex. In addition, neither positive nor negative symptoms systematically correlated with the cognitive deficits reported despite specific predictions from the current literature.
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PMID:Cognitive deficits in schizophrenia on the WAIS-R NI Sentence Arrangement Subtest. Wechsler Adult Intelligence Scale-Revised Neuropsychological Inventory. 1057 23

According to the ICD 10 only acute psychotic disorders and transitory acute disorders are specified, whereas DSM IV index, in the same class, schizophreniform disorder, schizoaffectif disorder and atypical psychosis. State biological markers of these disorders are present during the acute episode and disappear with it. A few studies concerns trait predispositional markers of these acute psychotic disorders. In addition, several studies of acute psychotic states are indexed as a partition of usual schizophrenic disorder, as a simple occurrence of that chronic disease. From the biological point of view, dysfunctions of norepinephrine and dopaminergic metabolisms are reported within these acute schizophrenic disorganisation, especially hyperdopaminergia, causality, consequence or evidence of the state syndrome. Those kinds of data are also reported in mood disorder with delusional symptoms. A hypothetic dysregulation of the balance between oxydation and antioxydation system has been searched in these acute states of schizophrenia. From the electrophysiologic perspective, no abnormalities are found for ocular movement functions during these acute psychotic disorders. Besides the clouding of consciousness of confusional states, neuropsychological abnormalities are reported: attention disorders, lack of inhibition of non relevant informations, abnormalities of working memory. Brain imaging can substantiate a diminution of the caudate nucleus size and a possible increase of D2 receptors number. Also, in these acute psychotic states abnormalities of humoral and cellular immunologic system have been found. Lastly, street drugs can originate confusional states and depersonalization, through their serotoninergic, dopaminergic and anticholinergic properties. Ethical drugs can also create an acute psychosis disorder: individual vulnerability and somatic disease cooccurrence act as risk-factors.
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PMID:[Biological approaches to acute psychoses]. 1059 92

Knowledge of the relationship between specific cognitive abnormalities and the clinical symptoms of schizophrenia could give insight into the nature of their underlying pathophysiology. Composite scores were generated for negative, disorganized, and psychotic symptom ratings in 134 patients with schizophrenia (DSM-IV criteria). Partial correlations (each composite corrected for the others) were computed with neuropsychological measures. Negative symptoms were related to poor performance on tests of verbal learning and memory, verbal fluency, visual memory, and visual-motor sequencing. Disorganized symptoms were correlated with lower verbal IQ and poor concept attainment. Psychotic symptoms had no significant relationship with cognitive deficit.
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PMID:Cognitive correlates of the negative, disorganized, and psychotic symptom dimensions of schizophrenia. 1067 6

Impairments in verbal learning and memory functioning have been found to be cardinal features among individuals with schizophrenia as well as among non-schizophrenic cocaine abusers. Cognitive deficits in these areas, moreover, have been associated with poor treatment response and short-term outcome. Little is known, however, about the acute effects of cocaine abuse on schizophrenic patients' learning and memory functioning. Consequently, a potentially reversible and treatable source of cognitive impairment has been virtually ignored. The present study examined the extent of verbal learning and memory impairment in a group of cocaine-dependent schizophrenic patients (n=42) and a group of non-schizophrenic cocaine-dependent patients (n=21) within 72 h of the last cocaine use using the California Verbal Learning Test (CVLT). Schizophrenic patients (n=34) without any substance-use disorders were also tested in an identical time frame and served as a comparison group. Results revealed that all groups demonstrated significant learning and memory impairment relative to CVLT published age and gender corrected norms. Both cocaine-dependent and non-substance abusing schizophrenic groups presented a very similar pattern of impaired learning and recall performance across all CVLT task domains. Comorbid patients, in contrast, presented with marked deficits in their ability to learn and recall verbal information relative to either schizophrenic or cocaine-only groups. Moreover, the cocaine-abusing schizophrenic patients showed significant forgetfulness of the information that they did acquire during delayed recall conditions. The performance deficits exhibited by cocaine-abusing schizophrenic patients differed not only in relative severity of impairment, but also qualitatively in their increased rates of forgetfulness of acquired information. These results are interpreted in terms of the neurobiological substrates of learning and memory and the neurobiological impact of cocaine on schizophrenic patients' cognition during the early phase of inpatient hospitalization. These results suggest that comorbid patients should be targeted for specialized remediation efforts at the beginning phases of inpatient treatment.
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PMID:Learning and memory impairment in cocaine-dependent and comorbid schizophrenic patients. 1069 25

Enlarged cavum septi pellucidi (CSP) is a neurodevelopmental anomaly that has been associated with schizophrenia. This study was designed to evaluate, in patients with schizophrenia, the relationship between the severity of this anomaly and measures of symptom and cognitive skills. Three groups were used: patients with large CSP (n=14), patients without large CSP (n=14), and healthy control subjects (n=14). In patients with large CSP, a significant, inverse relationship was found between size of CSP and measures of cognitive deficit. Thus, the greater the size of the anomaly, the greater the cognitive deficit. No relationship was found between severity of CSP and symptom measures.
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PMID:Enlarged cavum septi pellucidi in patients with schizophrenia: clinical and cognitive correlates. 1095 67

Microinjection of a serotonergic 5-HT1B agonist (S-CM-GTNH2, 3 microg/l) into the dorsal subiculum (DS) induced long-lasting increases in dopamine (DA; +58%), dihydroxyphenylacetic acid (DOPAC; +15%) and homovanillic acid (HVA; +31%), without changing extracellular levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), measured by microdialysis in freely moving rats in the shell area of the nucleus accumbens (n. acc). Perfusion of a glutamate-N-methyl-D-aspartate (NMDA) receptor antagonist (MK 801, dizocilpine, 10 microM) through the dialysis probe in the n. acc induced similar long-lasting increases in DA and DOPAC, whereas the glutamate-quisqualate/kainate receptor antagonist (CNQX, 50 microM) had no effect. In the presence of dizocilpine in the n. acc, microinjection of S-CM-GTNH2 into the DS could still increase DOPAC and HVA, but DA levels were not further changed, whereas in the presence of CNQX, microinjection of S-CM-GTNH2 into the DS still increased not only DOPAC and HVA, but also DA levels in a way similar to that in the absence of glutamate antagonist. Therefore, activation of 5-HT1B receptors located in the DS increases the release of DA in the n. acc, presumably via the glutamatergic projection to this structure and acting through NMDA receptors in it. This implies either the suppression of a tonic indirect inhibitory influence and/or stimulation of a phasic excitatory effect of glutamate. Disruption of latent inhibition (LI) has been suggested as a model for a cognitive deficit in schizophrenia (hyperattention to irrelevant stimuli) and is usually associated with an increase in DA release in the n. acc. However, s.c. injection of RU 24 969 (0.5 mg/kg), a mixed 5-HT1A-5-HT1B agonist, which was previously shown to increase DA release in the n. acc, left LI unchanged. Moreover, bilateral microinjections of S-CM-GTNH2 into the rat DS tended to potentiate LI, in spite of the increase in DA in n. acc demonstrated here. It is concluded that not all increases in DA release in the n. acc are functionally equivalent. Sensitization of receptors or impulse-dependent increase in DA release might be necessary to disrupt LI. The possible role of altered serotonergic transmission, through h5-HT1B receptors (human homologue of the rat 5-HT1B receptors) located in the DS, in acute schizophrenia needs to be further investigated.
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PMID:Dopamine release in the nucleus accumbens and latent inhibition in the rat following microinjections of a 5-HT1B agonist into the dorsal subiculum: implications for schizophrenia. 1095 52


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