Neurocognitive Effectiveness of Haloperidol, Risperidone, and Olanzapine in First-Episode Psychosis

Crespo‐Facorro, Benedicto; Rodríguez-Sánchez, José Manuel; Pérez-Iglesias, Rocí­o; Mata, Ignacio; Ayesa, Rosa; Ramírez-Bonilla, Mariluz; Martínez-Garcia, Obdulia; Vázquez‐Barquero, José Luís

doi:10.4088/jcp.08m04634

Cited by 57 publications

(43 citation statements)

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“…Recently, we reported that chronic administration of olanzapine reduces AA turnover, COX activity and pro-inflammatory PGE 2 concentrations in the rat brain (Cheon et al, 2011). Olanzapine has been shown to improve cognitive functioning in SZ patients after long-term treatment (Crespo-Facorro et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in the postmortem frontal cortex from schizophrenia patients

Rao

Kim

Harry

et al. 2013

Schizophrenia Research

100

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Schizophrenia (SZ) is a progressive, neuropsychiatric disorder associated with cognitive impairment. A number of brain alterations have been linked to cognitive impairment, including neuroinflammation, excitotoxicity, increased arachidonic acid (AA) signaling and reduced synaptic protein. On this basis, we tested the hypothesis that SZ pathology is associated with these pathological brain changes. To do this, we examined postmortem frontal cortex from 10 SZ patients and 10 controls and measured protein and mRNA levels of cytokines, and astroglial, microglial, neuroinflammatory excitotoxic, AA cascade, apoptotic and synaptic markers. Mean protein and mRNA levels of interleukin-1β, tumor necrosis factor-α, glial acidic fibrillary protein (GFAP), a microglial marker CD11b, and nuclear factor kappa B subunits were significantly increased in SZ compared with control brain. Protein and mRNA levels of cytosolic and secretory phospholipase A2 and cyclooxygenase were significantly elevated in postmortem brains from SZ patients. N-methyl-D-aspartate receptor subunits 1 and 2B, inducible nitric oxide synthase and c-FOS were not significantly different. In addition, reduced protein and mRNA levels of brain-derived neurotrophic factor, synaptophysin and drebrin were found in SZ compared with control frontal cortex. Increased neuroinflammation and AA cascade enzyme markers with synaptic protein loss could promote disease progression and cognitive defects in SZ patients. Drugs that downregulate these changes might be considered for new therapies in SZ.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in the postmortem frontal cortex from schizophrenia patients

Rao

Kim

Harry

et al. 2013

Schizophrenia Research

100

View full text Add to dashboard Cite

show abstract

“…of repeated exposure to the tests and/or assessment environment (i.e., retest effects) (Crespo-Facorro et al, 2009;Goldberg et al, 2010). To compare the retest effect on cognitive assessments, the control group was assessed at baseline and 8 weeks after the initial assessment.…”

Section: Methodsmentioning

confidence: 99%

“…The treatment interval in this study was 8 weeks, which is shorter than that used in other trials of SGAs in first-episode patients (Fagerlund et al, 2004;Goldberg et al, 2007;Crespo-Facorro et al, 2009;Andersen et al, 2011). It is possible that the ability of blonanserin to enhance cognitive functioning may have been greater if patients had been re-examined after a longer interval.…”

Section: Effect Of Blonanserin On Cognitive Functionmentioning

confidence: 97%

Retracted: Effect of blonanserin on cognitive function in antipsychotic‐naïve first‐episode schizophrenia

Tenjin

Miyamoto

Miyake

et al. 2012

Human Psychopharmacology

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“…Moreover, it has been suggested that the effects reported in some studies may have been biased by industry support (Heres et al, 2006), or methodological weaknesses (Harvey and Keefe, 2001). Other studies (Crespo-Facorro et al, 2009; Green et al, 2002; Harvey et al, 2005; Keefe et al, 2006; Rollnik et al, 2002) and meta-analyses (Mishara and Goldberg, 2004) have supported similar efficacy for FGA and SGA at improving cognition in schizophrenia. Several large-scale studies have reported the equal efficacy of FGA and SGA for treating cognitive disruption in schizophrenia (Jones et al, 2006; Keefe et al, 2007; Lewis et al, 2006).…”

Section: Introductionmentioning

confidence: 90%

Mouse pharmacological models of cognitive disruption relevant to schizophrenia

2012

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Schizophrenia is a debilitating cognitive disorder. The link between cognitive debilitation and functional outcome in patients with schizophrenia has prompted research to develop procognitive therapies. It is hoped that by improving cognition in these patients, their functional outcome will also improve. Although no established treatments exist as yet, progress has been made toward understanding how to evaluate putative compounds in the clinic. Genetic mouse models and pharmacological rat models of cognitive disruption are being developed that may help to evaluate these putative compounds preclinically. Considering the increased number of genetic mouse models relevant to schizophrenia, there is a need to evaluate pharmacological manipulations on cognition in mice. Here we review the current literature on mouse pharmacological models relevant to schizophrenia. In this review, we discuss where different pharmacological effects between rats and mice on cognitive tasks are observed and assess the validity offered by these models. We conclude that the predictive validity of these models is currently difficult to assess and that much more needs to be done to develop useful mouse pharmacological models of cognitive disruption in schizophrenia.

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Neurocognitive Effectiveness of Haloperidol, Risperidone, and Olanzapine in First-Episode Psychosis

Cited by 57 publications

References 0 publications

RETRACTED: Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in the postmortem frontal cortex from schizophrenia patients

RETRACTED: Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in the postmortem frontal cortex from schizophrenia patients

Retracted: Effect of blonanserin on cognitive function in antipsychotic‐naïve first‐episode schizophrenia

Mouse pharmacological models of cognitive disruption relevant to schizophrenia

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