Quetiapine regulates neurogenesis in ischemic mice by inhibiting NF-<i>κ</i>B p65/p50 expression

Bi, Xiaoying; Yan, Bin; Fang, Shaokuan; Yang, Yi; He, Jue; Li, Xinmin; Kong, Jiming

doi:10.1179/174313209x393573

Cited by 29 publications

(23 citation statements)

References 15 publications

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“…Contrary to findings in preclinical studies, quetiapine did not seem to protect against hippocampal volume loss (Bi et al 2009 ;Park et al 2006). No linear correlation between mean dose and volume loss was observed and the hippocampal volume loss appeared most pronounced in the high-dose group compared to HC.…”

Section: Discussioncontrasting

confidence: 77%

“…This has prompted the question as to whether antipsychotic compounds, and in particular SGAs, may protect against hippocampal volume loss (Angelucci et al 2000 ;Bai et al 2003 ;Halim et al 2004). In preclinical studies quetiapine has been shown to increase brain-derived neurotrophic factor (BDNF) expression (Park et al 2006 ;Xu et al 2002), to reduce neurodegeneration induced by global cerebral ischaemia (Bi et al 2009 ;Yan et al 2007), and to reverse stress-induced suppression of neurogenesis (Luo et al 2005) in hippocampus.…”

Section: Introductionmentioning

confidence: 99%

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Progressive striatal and hippocampal volume loss in initially antipsychotic-naive, first-episode schizophrenia patients treated with quetiapine: relationship to dose and symptoms

Ebdrup

Skimminge

Rasmussen

et al. 2010

Int. J. Neuropsychopharm.

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First-generation antipsychotics have been associated with striatal volume increases. The effects of secondgeneration antipsychotics (SGAs) on the striatum are unclear. Moreover, SGAs may have neuroprotective effects on the hippocampus. Dose-dependent volumetric effects of individual SGAs have scarcely been investigated. Here we investigated structural brain changes in antipsychotic-naive, first-episode schizophrenia patients after 6 months treatment with the SGA, quetiapine. We have recently reported on baseline volume reductions in the caudate nucleus and hippocampus. Baseline and follow-up T1-weighted images (3 T) from 22 patients and 28 matched healthy controls were analysed using tensor-based morphometry. Non-parametric voxel-wise group comparisons were performed. Small volume correction was employed for striatum, hippocampus and ventricles. Dose-dependent medication effects and associations with psychopathology were assessed. Patients had significant bilateral striatal and hippocampal loss over the 6-month treatment period. When compared to controls the striatal volume loss was most pronounced with low quetiapine doses and less apparent with high doses. Post-hoc analyses revealed that the striatal volume loss was most pronounced in the caudate and putamen, but not in accumbens. Conversely, hippocampal volume loss appeared more pronounced with high quetiapine doses than with low doses. Clinically, higher baseline positive symptoms were associated with more striatal and hippocampal loss over time. Although patients' ventricles did not change significantly, ventricular increases correlated with less improvement of negative symptoms. Progressive regional volume loss in quetiapine-treated, first-episode schizophrenia patients may be dose-dependent and clinically relevant. The mechanisms underlying progressive brain changes, specific antipsychotic compounds and clinical symptoms warrant further research.

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Section: Discussioncontrasting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Progressive striatal and hippocampal volume loss in initially antipsychotic-naive, first-episode schizophrenia patients treated with quetiapine: relationship to dose and symptoms

Ebdrup

Skimminge

Rasmussen

et al. 2010

Int. J. Neuropsychopharm.

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“…Moreover no increased risk of cerebrovascular events had been documented during atypical neuroleptic treatment (e.g risperidone or olanzapine) [37]. In experimental animal models of cerebral ischemia the olanzapine, risperidone, and quietapine showed evidence for neuroprotection after permanent focal cerebral ischemia [38-40]. …”

Section: Hemichorea-hemiballism Dystoniamentioning

confidence: 99%

Post-stroke Movement Disorders: Clinical Manifestations and Pharmacological Management

Siniscalchi¹,

Gallelli²,

Labate³

et al. 2012

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Involuntary abnormal movements have been reported after ischaemic and haemorrhagic stroke. Post stroke movement disorders can appear as acute or delayed sequel. At the moment, for many of these disorders the knowledge of pharmacological treatment is still inadequate. Dopaminergic and GABAergic systems may be mainly involved in post-stroke movement disorders. This article provides a review on drugs commonly used in post-stroke movement disorders, given that some post-stroke movement disorders have shown a partial benefit with pharmacological approach.

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“…[1–3]. Neuron-specific enolase and neuroglial mark-protein S-100 can reflect the degree of cerebral injury [4–6].…”

Section: Introductionmentioning

confidence: 99%

Primary Study for the Therapeutic Dose and Time Window of Picroside II in Treating Cerebral Ischemic Injury in Rats

Pei

Zhao

et al. 2012

IJMS

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The aim of this study was to explore the optimal therapeutic dose and time window of picroside II for treating cerebral ischemic injury in rats according to the orthogonal test. The middle cerebral artery occlusion (MCAO) models were established by intraluminally inserting a thread into middle cerebral artery (MCA) from left external carotid artery (ECA). The successful rat models were randomly divided into 16 groups according to the orthogonal layout of [L16(45)] and treated by injecting picroside II intraperitoneally with different doses at various times. The neurological behavioral function was evaluated by Bederson’s test and the cerebral infarction volume was measured by tetrazolium chloride (TTC) staining. The expressions of neuron specific enolase (NSE) and neuroglial mark-protein S-100 were determined by immunohistochemisty assay. The results indicated that the optimal compositions of the therapeutic dose and time window of picroside II in treating cerebral ischemic injury were ischemia 1.5 h with 20 mg/kg body weight according to Bederson’s test, 1.0 h with 20 mg/kg body weight according to cerebral infarction volume, 1.5 h with 20 mg/kg body weight according to the expressions of NSE and S-100 respectively. Based on the principle of the minimization of medication dose and maximization of therapeutic time window, the optimal composition of the therapeutic dose and time window of picroside II in treating cerebral ischemic injury should be achieved by injecting picroside II intraperitoneally with 20 mg/kg body weight at ischemia 1.5 h.

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Quetiapine regulates neurogenesis in ischemic mice by inhibiting NF-κB p65/p50 expression

Abstract: NF-kappaB plays a key role in regulating neuron damage and neurogenesis. This work suggests that down-regulation of NF-kappaB expression may be one of the mechanisms by which quetiapine inhibits neurogenesis.

Cited by 29 publications

References 15 publications

Progressive striatal and hippocampal volume loss in initially antipsychotic-naive, first-episode schizophrenia patients treated with quetiapine: relationship to dose and symptoms

Progressive striatal and hippocampal volume loss in initially antipsychotic-naive, first-episode schizophrenia patients treated with quetiapine: relationship to dose and symptoms

Post-stroke Movement Disorders: Clinical Manifestations and Pharmacological Management

Primary Study for the Therapeutic Dose and Time Window of Picroside II in Treating Cerebral Ischemic Injury in Rats

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