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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clozapine is an effective atypical antipsychotic drug used to treat schizophrenia. It has the advantage of producing fewer extrapyramidal motor side effects than typical antipsychotic drugs such as haloperidol. Schizophrenia involves more than the hallmark symptom of psychosis. Substantial cognitive impairment is also seen. Effective drug treatments against the cognitive impairment of schizophrenia need to be developed. The current study was conducted to determine the effects of clozapine on working memory in the rat neonatal hippocampal lesion model of schizophrenia, which includes symptoms of cognitive impairment. Infant Sprague-Dawley rats were given ibotenic acid lesions of the hippocampus on day 7 of age (using the day of birth as day 0). Controls were given vehicle infusions. In adulthood, the rats were trained on the 8-arm radial maze using the win-shift procedure. After 6 sessions of training, the lesioned rats and their controls were administered repeated injections of saline or clozapine (2.5 mg/kg) for the next 12 sessions of training. The females had significant radial-arm maze choice accuracy impairments caused by either clozapine or the hippocampal lesion, but the combination of the two treatments had no additive effect. The males showed a different pattern of effects. Intact males did not show a significant clozapine-induced impairment, whereas males with hippocampal lesions did show significant clozapine-induced impairment although hippocampal lesions by themselves did not significantly impair male choice accuracy. These data show that clozapine can cause memory impairment and it potentiates rather than reverses hippocampal lesion-induced deficits. There are critical sex-related differences in these effects.
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PMID:Effects of clozapine on memory function in the rat neonatal hippocampal lesion model of schizophrenia. 1635 17

Quetiapine, a new atypical antipsychotic drug, effectively alleviates positive and negative symptoms, as well as cognitive impairment that may be caused by neurodegeneration, in schizophrenia patients. Earlier in vivo and in vitro studies have demonstrated that quetiapine may be a neuroprotectant. The present study was designed to examine the beneficial effects of quetiapine on the possible cognitive impairment and changes of brain apoptotic regulation proteins induced by phencyclidine (PCP) in rats. Rats were treated with quetiapine (10 mg/kg/day; intraperitoneal (i.p.)) or vehicle for 16 days. On day 14, 1 h after the administration of quetiapine, the rats were given PCP (50 mg/kg; subcutaneous (s.c.)) or vehicle. Then quetiapine was administrated for an additional 2 days. One day after the last quetiapine injection (3 days after the PCP injection), the rats were trained on a spatial memory task in a radial arm maze. After the behavioural test, the rats were decapitated for Western blot analysis. PCP induced reference memory impairment, and a decrease of the ratio of an anti-apoptotic Bcl-2 family member (Bcl-XL) to a pro-apoptotic analogue (Bax) in the posterior cingulate cortex. Chronic administration of quetiapine counteracted the PCP-induced reference memory impairment and decrease of Bcl-XL/Bax ratio in the posterior cingulate cortex. These results suggest that quetiapine may have ameliorating effects on the cognitive impairment and brain apoptotic processes induced by PCP.
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PMID:The effects of chronic administration of quetiapine on the phencyclidine-induced reference memory impairment and decrease of Bcl-XL/Bax ratio in the posterior cingulate cortex in rats. 1636 Aug 89

Drug models of mental illness are considered useful if they provoke its characteristic symptoms. In this respect, ketamine and tetrahydrocannabinol (cannabis) are coming under increasing scrutiny as models for schizophrenia. However, although both undoubtedly produce psychotic symptoms characteristic of the disorder, we argue here that, because schizophrenia is also accompanied by cognitive deficits, a full understanding of the impact of these drugs on cognition will be crucial in taking these models further. Memory deficits are pronounced in schizophrenia and we focus upon patterns of working and episodic memory impairment produced by ketamine and cannabis, identifying overlaps between drug and illness. We suggest that close attention to these deficits can offer insights into core pathophysiology of schizophrenia.
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PMID:Schizophrenia, ketamine and cannabis: evidence of overlapping memory deficits. 1653 Oct 99

Source memory is impaired in schizophrenia, and this deficit is related to symptoms of interpersonal antagonism such as suspiciousness and hostility. The present study evaluated source memory in borderline personality disorder (BPD) and its relation to interpersonal antagonism. Forty-one noninpatient adults with BPD according to the DSM-IV and 26 healthy control subjects performed a verbal source memory test requiring completion of sentences with and without emotional content ("Hot" vs. "Cold" sentences). Subjects also completed self-report measures of suspiciousness and interpersonal antagonism (Buss-Durkee Hostility Inventory) and depression (Beck Depression Inventory). The BPD group showed no significant difference from the control group in self-referential source memory, recognition memory, response bias, and performance enhancement for items with emotion content. However, in the BPD group, poorer self-referential source memory was significantly related to Hostility measures including suspiciousness, but not with Depression scores. In contrast, generic item recognition memory was unrelated to Hostility. Heterogeneity in source memory function may be specifically related to some of the hallmark interpersonal disturbances of BPD, independent of the effects of general negative affect or general memory impairment.
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PMID:Reduced Self-Referential Source Memory Performance is Associated with Interpersonal Dysfunction in Borderline Personality Disorder. 1656 78

The role of slowing of processing speed in verbal memory impairment in patients with schizophrenia was investigated. Forty-one patients with schizophrenia and 41 healthy control subjects were administered a verbal memory task involving free recall of three lists of words, which varied in their degree of semantic organization. Standard processing speed tests were administered as well. Regression analyses were conducted on the number of words recalled in each list. A global processing speed measure was a significant predictor of the recall of each list in patients. Patients were very significantly impaired in the recall of the three lists relative to healthy controls. However, when the processing speed measure was entered in the regression, the significance of diagnosis was considerably reduced for one of the lists, with no semantic organization, and eliminated for the other two lists which contained semantic organization. These findings suggest that slowing in processing speed is an important contributor to verbal memory impairment in patients with schizophrenia. The possible role of various specific slowing functions is discussed.
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PMID:Processing speed: a strong predictor of verbal memory performance in schizophrenia. 1661 26

The purpose of this study was to investigate compromised memory function of schizophrenia patients in comparison with temporal lobe epilepsy patients, whose memory impairments result from a clear lesion. The authors hypothesized that schizophrenia patients would show poorer immediate and delayed recall performances in verbal and visual memory tasks. The study sample consisted of a healthy comparison group of 30 subjects and three patient groups comprising 76 schizophrenia patients, 93 left temporal lobe epilepsy patients, and 72 right temporal lobe epilepsy patients. The authors assessed immediate recall, delayed recall, and delayed retention. Tasks were subdivided into two categories (easy and difficult), and then patient memory dysfunction was compared among the memory tests. The authors observed material-specific memory impairment, where the left temporal lobe epilepsy group showed severe verbal memory impairment and the right temporal lobe epilepsy group showed severe visual memory impairment. A moderate impairment was found in immediate and delayed verbal memory in schizophrenia patients, and the impairment of visual memory was amplified with delayed recall. Such a result can be interpreted not only as a generalized cognitive deficit, but also as an integrative dysfunction involving the mesial temporal and frontal lobes in the left and right hemispheres, whereby the lesion site cannot be determined selectively. Our results show that the selection of a memory task that cannot be influenced by verbal mediation is very important for analyzing memory dysfunction in schizophrenia patients.
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PMID:Compromised memory function in schizophrenia and temporal lobe epilepsy. 1672 Jul 97

The ability to monitor memory performance has considerable importance in everyday life and is among the proposed metamemory dimensions which has been widely investigated. The ability to monitor memory performance accurately was examined in 16 patients with schizophrenia and 16 control subjects by using a Feeling-of-Knowing task on episodic information. Feeling-of-Knowing judgments are predictions made about the likelihood of subsequent recognition of currently non-recallable information. Participants were given cued recall and recognition tests of 50 sentence-target words. Feeling-of-knowing judgments were made for non-recalled targets. Our results first confirm that schizophrenia is associated with episodic memory impairment. By using the Feeling-of-Knowing task, patients with schizophrenia were found to predict accurately their subsequent recognition performance, suggesting an interesting dissociation between a preserved metamemory and an altered memory.
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PMID:Metamemory in Schizophrenia: an exploration of the feeling-of-knowing state. 1672 27

Transient working memory requires attention and temporary storage of information, whereas executive function working memory requires additional mental manipulation of that information. Working memory impairment is common in schizophrenia patients, but only some studies have found differential impairment in executive function working memory compared to transient working memory. We measured both types of working memory using the Digit Span forward (DF) and backward (DB) tasks in a large sample of schizophrenia patients (n=267) and normal comparison subjects (n=82); in the patients, we also examined associations between performance on the Digit Span tasks and Letter-Number Sequencing (LNS), a putative executive function working memory test. Compared to healthy subjects, the schizophrenia patients showed impairment in the medium effect size range on both DF (d=-0.55) and DB (d=-0.68). DB scores predicted LNS performance, whereas DF scores did not. Worse negative symptoms were associated with worse performance on DF, DB and LNS. These results do not reflect differential executive function working memory dysfunction in schizophrenia, but appear to support transient and executive function working memory as separable constructs.
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PMID:Transient and executive function working memory in schizophrenia. 1673

Perinatal asphyxia occurs in approximately 1-6 per 1000 live full-term births. Different patterns of brain damage can result, though the relation of these patterns to long-term cognitive-behavioural outcome remains under investigation. The hippocampus is one brain region that can be damaged (typically not in isolation), and this site of damage has been implicated in two different long-term outcomes, cognitive memory impairment and the psychiatric disorder schizophrenia. Factors in addition to the acute episode of asphyxia likely contribute to these specific outcomes, making prediction difficult. Future studies that better document long-term cognitive-behavioural outcome, quantitatively identify patterns of brain injury over development and consider additional variables that may modulate the impact of asphyxia on cognitive and behavioural function will forward the goals of predicting long-term outcome and understanding the mechanisms by which it unfolds.
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PMID:Brain and cognitive-behavioural development after asphyxia at term birth. 1676 8

Patients with schizophrenia exhibit deficits in a range of cognitive functions, particularly working and episodic memory, which are thought to be core features of the disorder. Memory dysfunction in schizophrenia is familial and thus a promising endophenotype for genetic studies. Both human and animal studies suggest a role for the neural nicotinic acid receptor family in cognition and specifically the alpha7-receptor subunit in schizophrenia and its endophenotypes. Consequently, we tested mice lacking the alpha7 subunit of the neural nicotinic receptor (B6.129S7-Chrna7(tm1Bay)/J) in the delayed matching-to-place (DMP) task of the Morris water maze, a measure of working/episodic memory akin to human episodic memory. We report that a minor impairment in alpha7 knockout mice was observed in the DMP task, with knockout mice taking longer to find the hidden platform than their wildtype controls. This suggests a role for the alpha7 subunit in working/episodic memory and a potential role for the alpha7 neural nicotinic receptor gene (CHRNA7) in schizophrenia and its endophenotypes.
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PMID:Performance deficit of alpha7 nicotinic receptor knockout mice in a delayed matching-to-place task suggests a mild impairment of working/episodic-like memory. 1692 47


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