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MicroRNA137 (miRNA137) regulates several gene expressions involved in brain development, and a recent large genome wide association study (GWAS) revealed a possible association between miRNA137 and schizophrenia.
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Atypical antipsychotic drugs offer several notable benefits over typical antipsychotics, including greater improvement in negative symptoms, cognitive function, prevention of deterioration, and quality of life, and fewer extrapyramidal symptoms (EPS). However, concerns about EPS have been replaced by concerns about other side effects, such as weight gain, glucose dysregulation and dyslipidemia. These side effects are associated with potential long-term cardiovascular health risks, decreased medication adherence, and may eventually lead to clinical deterioration. Despite a greater understanding of the biochemical effects of these drugs in recent years, the pharmacological mechanisms underlying their various therapeutic properties and related side effects remain unclear. Besides dopamine D(2) receptor antagonism, a characteristic feature of all atypical antipsychotic drugs, these agents also bind to a range of non-dopaminergic targets, including serotonin, glutamate, histamine, alpha-adrenergic and muscarinic receptors. This review examines the potential contribution of different receptors to metabolic side effects associated with atypical antipsychotic treatment for all seven agents currently marketed in the United States (risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, paliperidone and clozapine) and another agent (bifeprunox) in clinical development at the time of this publication.
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We conclude that there is limited evidence to support the use of some atypical antipsychotics and other medications for NPS in LTC populations. However, the generally modest efficacy and risks of adverse events highlight the need for the development of safe and effective pharmacological and non-pharmacological interventions for this population.
The liquid-liquid extraction and UHPLC-MS/MS technique allows robust target screening and quantification of 23 antipsychotics and metabolites.
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Eight hundred thirty-four adult patients were included in this study, of whom 130 used aripiprazole, 312 used haloperidol, 86 used pimozide, and 396 used risperidone. Serum levels of the drug and, if available, their active metabolites were collected as well as information on dose. Patients were genotyped for CYP3A4*22 using restriction fragment length polymorphism analysis. Genotyping for CYP2D6 was done with allele-specific polymerase chain reaction.
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Cariprazine, as well as aripiprazole and bifeprunox, were able to reduce the rewarding effect of cocaine (minimum effective doses were 0.17, 1, and 0.1 mg/kg, respectively) and attenuated relapse to cocaine seeking with half maximal effective dose [ED₅₀] values of 0.2, 4.2, and 0.17 mg/kg, respectively.
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Autism spectrum disorder is a diagnosis that includes significant social communication deficits/delays along with restricted patterns of interests and behaviors. The prevalence of this diagnosis has increased over the past few decades, and it is unclear whether this is solely attributable to the increased awareness of milder forms of the disorder among medical providers. The current treatment options for the core symptoms of autism are limited to psychosocial therapies, such as applied behavior analysis. Medications have been most effective in treating the associated behavioral symptoms of autism, though studies have examined potential benefits in some of the core symptoms of autism with certain medications, especially the repetitive behaviors often seen with this diagnosis. Risperidone and aripiprazole are currently the only medications FDA approved for symptoms associated with autism spectrum disorders, targeting the irritability often seen with this diagnosis. Children and adolescents with autism spectrum disorder appear to be more susceptible to adverse effects with medications; therefore, initiation with low doses and titrating very slowly is recommended. Some complementary alternative treatments have been researched as possible treatments in autism, though evidence supporting many of these is very limited.
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We review evidence from randomized, placebo-controlled studies of patients with schizophrenia or schizoaffective disorder, which compared 2 or more doses of an antipsychotic to calculate the dose-response curve for each first-generation (typical) antipsychotic (FGA) or second-generation (atypical) antipsychotic (SGA) and as a group (based on dose equivalence). We identified the near-maximal effective dose (ED; ie, the threshold dose necessary to produce all or almost all the clinical responses for each drug). In randomized, fixed-dose studies of SGAs, the near-maximal efficacy dose for olanzapine may be greater than 16 mg; for risperidone, it is 4 mg; and for ziprasidone, it is 120 mg. Risperidone at 2 mg daily is 50% less efficacious than higher doses. Olanzapine at about 6 mg is approximately 33% less effective than higher doses. Aripiprazole at 10 mg daily was fully efficacious. Doses of clozapine well above 400 mg are necessary for optimal treatment of many schizophrenia patients. We found 3.3 to 10 mg haloperidol to be the near-maximal ED range. We find no evidence that doses higher than these are more effective. We failed to find that high doses of haloperidol (or all other first-generation comparison drugs converted to equivalent doses) were less effective than medium doses (3.3 to 10 mg). While high-dose FGAs are not less effective, we feel it is important not to avoid using high dose to avoid excessive toxicity.
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Antipsychotics are the cornerstone for the maintenance treatment of schizophrenia patients. Their long-acting formulations are helpful for preventing relapses through improvement of adherence to medication and a better pharmacokinetic coverage. However, their use is often reserved for refractory or non-observant clinical forms because of limitations among both clinicians and patients. The development of a new formulation of long-acting injectable aripiprazole administered every 4 weeks is a new option. Two randomized controlled trials vs. placebo and vs. oral aripiprazole respectively show a superiority and non-inferiority in terms of relapse prevention. Meanwhile, a mirror-image study demonstrates fewer hospitalizations. The safety profile is comparable to the oral formulation, particularly in terms of metabolic and neurological side-effects. As mentioned in various professional recommendations, long-acting injectable antipsychotics, so long-acting injectable aripiprazole, are one of the major strategies of the maintenance treatment for patients with schizophrenia.
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This two-year, rater-blinded, open-label, multicenter study (NCT00299702) randomized subjects to injectable risperidone long-acting therapy (25-50mg, injected every 2 weeks) or oral aripiprazole (5-30mg/day), with study visits every two weeks. Subjects who met relapse criteria or discontinued study drug could remain in the study.
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We identified 21 studies of drug versus placebo that met the inclusion criteria, with a total of 2,455 patients, 14 studies for risperidone (1,331 patients), three for olanzapine (276 patients), and four for aripiprazole (848 patients). Compared with placebo, the mean weight increases for each drug were olanzapine 3.45 kg (95 % CI 2.93-3.98), risperidone 1.77 kg (95 % CI 1.35-2.20), and aripiprazole 0.94 kg (95 % CI 0.65-1.24). Regarding other metabolic abnormalities, eight studies reported statistically significant increases in prolactin with risperidone; two reported a statistically significant increase in glucose, total cholesterol, and prolactin with olanzapine; and three studies reported a statistically significant decrease in prolactin with aripiprazole. Data on lipid, glucose, and prolactin level changes were too limited to allow us to perform a meta-analysis.
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323 subjects being treated with either risperidone (n = 177) or quetiapine (n = 146) were randomly assigned to receive adjunctive aripiprazole (n = 168) or placebo (n = 155). Baseline characteristics were similar (mean PANSS total score: aripiprazole, 74.5; placebo, 75.9) except for history of suicide attempts (aripiprazole, 27%; placebo, 40%). Nearly 70% of subjects in each arm completed the trial. Adjunctive aripiprazole and placebo groups were similar in the mean change from baseline to endpoint in the PANSS total score (aripiprazole, -8.8; placebo, -8.9; P = .942). The incidence of treatment-emergent adverse events was similar between groups. Mean changes in Simpson-Angus Scale, Abnormal Involuntary Movement Scale, and Barnes Akathisia Rating Scale scores were not statistically significantly different. Adjunctive aripiprazole was associated with statistically significantly greater decreases in mean serum prolactin levels from baseline than was adjunctive placebo (-12.6 ng/mL for aripiprazole vs -2.2 ng/mL for placebo; P < .001), an effect that was seen in the risperidone subgroup (-18.7 ng/mL vs -1.9 ng/mL; P < .001) but not in the quetiapine subgroup (-3.01 ng/mL vs +0.15 ng/mL; P = .104).
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The findings from this open-label study suggest that the neurocognitive effects of aripiprazole are at least as good as those of olanzapine.
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Although emotional dysfunction in patients with schizophrenia is thought to be associated with poorer outcomes in terms of overall quality of well-being, only a few basic studies have been done on the biochemical effect of antipsychotics on the fear response of a neurotransmitter (i.e. dopamine). To examine the reaction to emotional stress, conditioned fear stress has been developed as a form of psychological stress based on classical conditioning theory. Using this model, the amygdala was found to be one of the most potent modulators of the mechanisms responsible for the emotional memory system. Methamphetamine-induced sensitization (reverse tolerance phenomenon) in rats has been widely and successfully used as an animal model of stimulant-induced psychosis and schizophrenia in terms of the paranoid psychotic state and its vulnerability to relapse. Methamphetamine-sensitized animals show significantly higher extracellular dopamine release in the amygdala than unsensitized rats after exposure to a conditioned stimulus. This hypersensitivity of dopamine release is considered to be a biochemical marker of hypersensitivity and vulnerability to stress in psychosis. Aripiprazole and haloperidol equally suppressed the marked increase in extracellular dopamine levels in fear-conditioned rats, whereas haloperidol increased and aripiprazole decreased basal dopamine levels. The effect of antipsychotics attenuates the dopamine fear response in the amygdala, modulating basal dopamine level.
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La depresión en la edad avanzada (DEA) es una preocupación creciente de salud general y pública, con diversas manifestaciones clínicas y etiologías. Este artículo revisa de manera resumida los hallazgos de las neuroimágenes asociados con la depresión en adultos mayores y la variabilidad de la respuesta terapéutica. La DEA se ha asociado con atrofia cerebral, disminución de la integridad de la mielina y lesiones cerebrales en las regiones límbicas-frontoestriatales. Estas asociaciones ayudan a explicar el síndrome de disfunción ejecutiva de la depresión observado en la DEA y apoyan la carga cerebrovascular como un mecanismo patogénico. Este artículo sugiere además que los hallazgos esenciales de las neuroimágenes de la resistencia al tratamiento también reflejan la carga cerebrovascular. Entre las teorías etiológicas de la DEA, la carga cerebrovascular puede mediar la resistencia al tratamiento. Esta revisión propone que las neuroimágenes tienen un potencial en la traslación clínica. Los ensayos controlados pueden identificar biomarcadores de neuroimágenes que orienten el tratamiento al identificar adultos con depresión que probablemente remitirán con farmacoterapia, identificar dosis terapéuticas individualizadas y facilitar las mediciones de respuesta terapéutica precoz. Las neuroimágenes también tienen el potencial de orientar de manera similar la variabilidad de la respuesta terapéutica del tratamiento con aripiprazol (modulador dopaminérgico) y con buprenorfina (modulador opiáceo).
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Depressive mood in adolescents with bipolar disorder (BDd) is associated with significant morbidity and mortality, but we have limited information about neural correlates of depression and treatment response in BDd. Ten adolescents with BDd (8 females, mean age = 15.6 ± 0.9) completed two (fearful and happy) face gender labeling fMRI experiments at baseline and after 6-weeks of open treatment. Whole-brain analysis was used at baseline to compare their neural activity with those of 10 age and sex-matched healthy controls (HC). For comparisons of the neural activity at baseline and after treatment of youth with BDd, region of interest analysis for dorsal/ventral prefrontal, anterior cingulate, and amygdala activity, and significant regions identified by wholebrain analysis between BDd and HC were analyzed. There was significant improvement in depression scores (mean percentage change on the Child Depression Rating Scale-Revised 57 % ± 28). Neural activity after treatment was decreased in left occipital cortex in the intense fearful experiment, but increased in left insula, left cerebellum, and right ventrolateral prefrontal cortex in the intense happy experiment. Greater improvement in depression was associated with baseline higher activity in ventral ACC to mild happy faces. Study sample size was relatively small for subgroup analysis and consisted of mainly female adolescents that were predominantly on psychotropic medications during scanning. Our results of reduced negative emotion processing versus increased positive emotion processing after treatment of depression (improvement of cognitive bias to negative and away from positive) are consistent with the improvement of depression according to Beck's cognitive theory.
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From October 2005 to January 2011 a prospective, randomized, open-label study was undertaken. 141 patients who were randomly allocated to aripiprazole (N=56), quetiapine (N=36) or ziprasidone (N=49) were analyzed. The main outcome was differences in prolactin plasma levels over 1year follow-up among the three antipsychotics. Prolactin levels had a skewed distribution and therefore they were log-transformed before statistical analyses.
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There are supportive evidences about the possible role of latent Toxoplasma. gondii infections on the behavior and neurologic functions, such as increased dopamine levels in the brain. The aim of this study was to examine anti-toxoplasma activity of aripiprazole that is an atypical anti-psychotic drug in mice.
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The effectiveness of aripiprazole treatment was demonstrated in a broad range of schizophrenia patients (CGI-I score of 3.0; 95% confidence interval: 2.8, 3.2: last observation carried forward [LOCF]) as the upper bound of the 95% CI was less than 4 (score of "no change"). Both patient and caregiver PGI-I scores (LOCF: 95% CI: 2.79, 3.09 and, 95% CI: 2.74, 3.17, respectively) corroborate this finding. Aripiprazole had a positive effect on disease severity by study end, as assessed by an increase of the (physician-rated) CGI-S scores, with 57.3% of patients having improved disease, one-third maintaining their condition (30.8%) and 11.3% with worsening symptoms (LOCF). The Investigator Assessment Questionnaire (IAQ) showed a great improvement (>50% of patients). Patients reported significantly improved quality of life and overall, 71% of patients and 67% of caregivers preferred aripiprazole to their previous antipsychotic medication (LOCF; P<0.0001 over time).
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The aim of this study was to determine the eff ectiveness and safety of aripiprazole in children and adolescents with both attention deficit/hyperactivity disorder (ADHD) and conduct disorder (CD).
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To evaluate utilization of 90-day-supply prescriptions of aripiprazole.
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To evaluate the cost-effectiveness of aripiprazole and olanzapine in patients with schizophrenia.
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At week 12, significantly more patients taking aripiprazole (49.7%) were in response and receiving therapy compared with those taking haloperidol (28.4%; P < 0.001). Continuation rates differed markedly between treatments (week 12: aripiprazole, 50.9%; haloperidol, 29.1%). Extrapyramidal adverse events were more frequent with haloperidol than aripiprazole (62.7% v. 24.0%).
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Antipsychotics (AP) induce weight gain. However, reviews and meta-analyses generally are restricted to second generation antipsychotics (SGA) and do not stratify for duration of AP use. It is hypothesised that patients gain more weight if duration of AP use is longer.
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Prolactin concentrations were significantly higher in women than in men (8.9 ± 7.5 vs 3.4 ± 3.0 ng/mL, P < 0.001). No correlations were found between prolactin concentrations and plasma concentrations of aripiprazole, dehydroaripiprazole or the sum of the two compounds. Prolactin concentrations were not affected by any polymorphism.
Medline/PubMed/Psyclit/Embase database searches were conducted in January 2015, and a manual review of references within the retrieved articles was done. All articles in English and those that had English abstracts and dealt with treatment of TDt were included.