Research and Clinical Trials on Quetiapine (Seroquel)

By Dr Greg Mulhauser
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This list of current clinical research trials on Quetiapine (Seroquel) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Quetiapine (Seroquel) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Quetiapine (Seroquel).

 

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Current Research Literature on Quetiapine (Seroquel)

Here are abstracts for some of the latest research articles to have appeared on Quetiapine (Seroquel):

Biological perspectives incarcerated care and quetiapine abuse.

Perspect Psychiatr Care. 2008 Jul; 44(3): 202-6
Keltner NL, Vance DE

Neuroleptic Malignant Syndrome Associated With Atypical Antipsychotics in Pediatric Patients: A Review of Published Cases.

J Clin Psychiatry. 2008 Jun 17; e1-e9
Croarkin PE, Emslie GJ, Mayes TL
OBJECTIVE: To retrospectively examine published cases of neuroleptic malignant syndrome (NMS) in patients aged 18 and below who had been treated with atypical antipsychotics (clozapine, risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole). DATA SOURCES: Information was collected via MEDLINE searches in February 2006 and May 2007. The term neuroleptic malignant syndrome was used and cross-referenced with individual atypical antipsychotics. The authors also contacted (by telephone and in writing) pharmaceutical companies that produce and market atypical antipsychotics for any data on NMS. STUDY SELECTION: Twenty case reports (written in English only and published from 1991-2007) were identified and reviewed. These publications all described symptoms of NMS in patients aged 18 or younger who had been treated with atypical antipsychotics. DATA EXTRACTION: Data were reviewed and compared with 3 diagnostic criteria (DSM-IV-TR, Levenson's, and Caroff and Mann's) for NMS. Interventions and outcomes were also reviewed. DATA SYNTHESIS: Twenty case reports were identified and presented with a descriptive approach. Sixteen cases met criteria for NMS, with at least 1 of the diagnostic sets utilized. The majority of cases involved male subjects. All patients recovered. CONCLUSIONS: Young patients can develop NMS during treatment with atypical antipsychotics. Symptoms of this disorder are consistent with those described in adults. Although NMS is rare in this population, clinicians should maintain a high index of suspicion. Appropriate caution in treating children and adolescents with any antipsychotic is warranted.

Weight change in Parkinson and Alzheimer patients taking atypical antipsychotic drugs.

J Neurol Sci. 2008 Jun 13;
Sitburana O, Rountree S, Ondo WG
Atypical antipsychotics (AA) are generally associated with weight gain. We determined body mass index (BMI) change in Parkinson's disease (PD) before and after taking AA and compared against PD controls and Alzheimer's disease (AD) patients on AA. In 66 consecutive PD subjects started on AA who had accurate weights for more than 6 months before and after initiation of AA, we compared weight change before and after AA use, against a control group of sixty-one sex-matched PD subjects, and against twenty-eight AD subjects taking AA. A linear regression model was created to compare weight changes. Fifty-nine PD subjects had complete data, quetiapine (n=53) and clozapine (n=6). The mean BMI change in the period before starting AA was 0.00 kg/m(2)/month over 1.95+/-1.41 years. After starting AA, subjects lost 0.03 kg/m(2)/month (95% CI 0.62-1.21, P

Demonstration of an anti-oxidative stress mechanism of quetiapine.

FEBS J. 2008 Jun 12;
Xu H, Wang H, Zhuang L, Yan B, Yu Y, Wei Z, Zhang Y, Dyck LE, Richardson SJ, He J, Li X, Kong J, Li XM
We have shown that quetiapine, a new antipsychotic drug, protects cultured cells against oxidative stress-related cytotoxicities induced by amyloid beta (Abeta)25-35, and that quetiapine prevents memory impairment and decreases Abeta plaques in the brains of amyloid precursor protein (APP)/presenilin-1 (PS-1) double-mutant mice. The aim of this study was to understand why quetiapine has these protective effects. Because the cytotoxicity of both Abeta(25-35) and Abeta(1-40) requires fibril formation, our first experiments determined the effect of quetiapine on Abeta(25-35) aggregation. Quetiapine inhibited Abeta(25-35) aggregation in cell-free aqueous solutions and blocked the fibrillar aggregation of Abeta(25-35), as observed under an electron microscope. We then investigated why quetiapine inhibits Abeta(25-35) aggregation. During the aggregation of Abeta(25-35), a hydroxyl radical (OH(*)) was released, which in turn amplified Abeta(25-35) aggregation. Quetiapine blocked OH(*)-induced Abeta(25-35) aggregation and scavenged the OH(*) produced in the Fenton system and in the Abeta(25-35) solution, as analyzed using electron paramagnetic resonance spectroscopy. Furthermore, new compounds formed by quetiapine and OH(*) were observed in MS analysis. Finally, we applied Abeta(25-35) to PC12 cells to observe the effect of quetiapine on living cells. Abeta(25-35) increased levels of intracellular reactive oxygen species and calcium in PC12 cells and caused cell death, but these toxic effects were prevented by quetiapine. These results demonstrate an anti-oxidative stress mechanism of quetiapine, which contributes to its protective effects observed in our previous studies and explains the effectiveness of this drug for Alzheimer's disease patients with psychiatric and behavioral complications.

Quetiapine and ziprasidone as adjuncts in treatment-resistant obsessive-compulsive disorder : a retrospective comparative study.

Clin Drug Investig. 2008; 28(7): 439-42
Savas HA, Yumru M, Ozen ME
BACKGROUND AND OBJECTIVE: While serotonin reuptake inhibitors (SRIs) are first-line pharmacological agents in the treatment of obsessive-compulsive disorder (OCD), 40-60% of patients with the disorder do not respond to these agents. This suggests that other neurotransmitters may play a role in OCD. In this regard, there has been particular interest in the dopaminergic system, with various antipsychotic drugs having been used as adjunctive therapy for refractory OCD. The aim of this study was to compare the efficacy of quetiapine and ziprasidone as adjuncts for treatment-resistant OCD. METHODS: A total of 24 OCD patients treated with either quetiapine (n = 15) or ziprasidone (n = 9) as adjunctive therapy to high-dose SRI treatment were included in this retrospective evaluation. Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and Clinical Global Impression (CGI) scale scores were used to evaluate baseline clinical status and clinical improvement at 1, 2, 3 and 6 months of follow-up. RESULTS: Clinical improvement was established in 80% of the quetiapine group and in 44.4% of the ziprasidone group with an overall mean improvement rate on the Y-BOCS scale of 66.7%. Both Y-BOCS and CGI mean scores were higher in the ziprasidone group at 2, 3 and 6 months follow-up than in the quetiapine group. CONCLUSIONS: In the first reported study of its role in this setting, ziprasidone was found to be less effective than quetiapine in the treatment of refractory OCD.

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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