Background: Autism spectrum disorders (ASD) are a group of complex developmental disabilities which can cause behavior, social, and communication deficits. Anti-psychotic medications are often prescribed when symptoms such as aggression, irritability, hyperactivity, tantrums, and self-injurious behavior occur. Objective: To determine if anti-psychotic medications improve the behavior, social, and communication symptoms associated with ASD in children and adolescents. Search Strategy: Electronic literature searches were performed to find relevant studies and utilized the (1) Cochrane Database of Systematic Reviews, (2) Hispanic American Periodicals Index, (3) Medline, (4) PAIS International, (5) ProQuest Dissertations and Theses, (6) PsycInfo, (7) PubMed, (8) Springer LINK, (9) Taylor and Francis Journals, and (10) Sage Premier. Selection Criteria: Randomized controlled trials (RCTs) or quasi-experimental design (QED) studies of any dose of an anti-psychotic medication compared to a placebo or other prescription drug, in participants with autism spectrum disorder. Data Collection and Analysis: All studies which met the full-text level criteria were reviewed by a third party to validate the decision of inclusion. Meta-analyses in this review implemented both random and fixed-effects models. Main Results: Ten RCTs were included. Six studies evaluated a drug versus a placebo and four studies investigated the effects of two separate anti-psychotic medications or the efficacy of an additive medication to a drug and placebo group. Author's Conclusions: Limited evidence suggests the effectiveness of anti-psychotic medications in treating the behavior, social, and associated with autism; however, further research is needed to determine the implications of long-term use.

Patients with schizophrenia are normally treated with one of several antipsychotic medications that differ from one another in the areas of the brain they affect including the dorsal striatum, a subcortical section of the forebrain, and the prefrontal cortex (PFC), located in the anterior part of the frontal lobes. Two different tests of implicit memory, the probabilistic classification learning (PCL) and the Iowa gambling task (IGT), have been shown to rely on the dorsal striatum and the PFC, respectively. Studies have previously shown that patients with schizophrenia treated with antipsychotics that affect the dorsal striatum (e.g., risperidone), have altered performance on the PCL, and those treated with antipsychotics that affect the PFC (e.g., clozapine), have altered performance on the IGT. We tested the hypothesis that patients with schizophrenia treated with olanzapine would have a poorer performance on the IGT, but not the PCL, when compared with controls. This study aimed to clarify conflicting results from prior experiments observing the effects of olanzapine on implicit memory in people with schizophrenia. We also hypothesized that performance of patients taking aripiprazole would be comparable to those taking risperidone, or an FGA; however, we were unable to recruit a sufficient amount of participants to test this hypothesis. Patients with schizophrenia, a mental disorder characterized by a breakdown in relation between thoughts, emotion, and behavior, treated with olanzapine were recruited through local psychiatric clinics or using a newspaper ad. Administration of the Brief Psychiatric Rating Scale (BPRS) and the Mini Mental State Examination (MMSE) preceded a brief questionnaire of demographic information. Participants were tested on the PCL and the IGT using a personal computer. Results revealed poorer performance on both the MMSE and BPRS for patients when compared with controls. Patients taking olanzapine were impaired in learning the PCL but not the IGT when compared with controls. Results suggest that olanzapine acts on the PFC to augment IGT performance but further studies are needed. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2013-07-23 15:09:21.55

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Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Parmi les tumeurs cérébrales primaires, les gliomes sont les tumeurs les plus fréquemment rencontrées. Les glioblastomes (GBM) représentent 60 à 70% de ces tumeurs et malgré de récents progrès dans leur traitement, leur pronostic reste sombre. Les gliomes malins sont caractérisés par une prolifération cellulaire importante, un taux élevé de néo-angiogenèse et une migration diffuse des cellules tumorales gliales dans le parenchyme cérébral, ce qui rend impossible une résection chirurgicale complète. De plus, les cellules gliales tumorales migrantes opposent une résistance particulière aux traitements chimiothérapiques de type pro-apoptotique, causant une récidive quasi inévitable de ce type de tumeur. La compréhension des aspects moléculaires à la base de la prolifération, de la migration et de la chimiorésitance des cellules gliales tumorales est donc essentielle pour élaborer des approches ciblées capables d’entraver ces processus. La littérature mentionne plusieurs stratégies qui permettraient, en théorie, de court-circuiter la résistance à l’apoptose des cellules tumorales gliales migrantes. Il s’agirait entre autres :<p>- de réduire le taux d’activation des voies de signalisation contrôlées par PI3K /Akt /mTOR et NFkappaB, qui diminuerait le taux de croissance des gliomes malins, ainsi que le taux de migration des cellules tumorales isolées dans le parenchyme cérébral;<p>- de réduire le taux de migration des cellules tumorales gliales afin de restaurer un certain degré de sensibilité à des agents chimiothérapiques pro-apoptotiques;<p>- d’endiguer l’export des agents chimiothérapiques par les pompes à efflux surexprimées dans les gliomes <p>- d'induire d’autres processus de mort cellulaire que l’apoptose, car les cellules tumorales gliales migrantes sont plus sensibles à d’autres formes de mort cellulaire.<p>Ces besoins de nouvelles stratégies thérapeutiques ont motivé ce travail qui se focalisera sur le potentiel antitumoral des ligands du R-sigma1 dans les glioblastomes. Ainsi, nous montrerons que les ligands des Rs-sigma sont capables de produire certains des effets visés dans les stratégies ci-dessus, dont la réduction de la prolifération et de la migration des cellules cancéreuses avec une certaine potentialisation des chimiothérapies. Ces propriétés ouvrent de nouvelles perspectives en thérapie anticancéreuse pour cette famille de ligands, dont plusieurs membres sont déjà utilisés depuis de nombreuses années comme antipsychotique. / Doctorat en Sciences biomédicales et pharmaceutiques / info:eu-repo/semantics/nonPublished

<p>Anti-psychotic drug (APD) administration can induce movement disorders including tardive dyskinesia (TD), characterized by abnormal movements of the oro-facial region and occasionally the trunk and limbs. The most widely accepted model of TD is the APD-induced vacuous chewing movement (VCM). While the mechanism of induction of TD remains unclear, there are two prevailing hypothesis: oxidative stress and dopamine supersensitivity. Currently available APDs antagonize dopamine D2 receptors (D2R) which can result in excessive dopamine accumulation and oxidation which was demonstrated to induce striatal neurodegeneration and increased oxidative stress. The dopamine supersensitivity hypothesis proposes that APD treatment causes an up-regulation of high affinity D2Rs to compensate for D2R antagonism. Curcumin, a derivative of turmeric, has been demonstrated to affect dopamine levels and hold significant anti-apoptotic potential. Thus, the goal of this study was to investigate curcumin’s potential to prevent haloperidol-induced behavioural and biochemical abnormalities. Four groups of rats were treated daily: control; haloperidol (at 2mg/kg intra-peritoneally); curcumin (at 200mg/kg orally in jello) and curcumin plus haloperidol. VCMs, catalepsy and locomotor activity were assessed. Animals were sacrificed and tissues removed for qPCR, immunoblot, receptor binding, and UPLC assessments. At day14 there was a significant increase in VCMs and catalepsy following haloperidol treatment, which was prevented by curcumin treatment. However, curcumin did not alter locomotor activity. Curcumin was demonstrated to increase the expression of the anti-apoptotic molecule BclXL and to increase striatal D2Rs. These investigations support the potential of curcumin in the prevention of TD and provide insight into the complex pathophysiology of this disorder.</p> / Doctor of Philosophy (Medical Science)