Brain-derived neurotrophic factor and schizophrenia

Carlo, Pasquale Di; Punzi, Giovanna; Ursini, Gianluca

doi:10.1097/ypg.0000000000000237

Cited by 84 publications

(65 citation statements)

References 98 publications

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“…Previous studies have shown that quetiapine attenuated the immobilization stress-induced decrease in expression of brain-derived neurotrophic factor (BDNF, a neuroprotective protein) ( 19 ), promoted neuroplasticity via the up-regulation of BDNF ( 20 ) in rat hippocampus, and modulated conditioned anxiety by affecting brain BDNF expression in Alzheimer’s transgenic mice ( 21 ). BDNF is relevant for schizophrenia-related phenotypes, and disruption of BDNF signaling is associated with altered synaptic plasticity and neurodevelopment of schizophrenia ( 22 ). Cerebral myelination can be evaluated by measuring the expression of myelin basic protein (MBP) ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Wen³

et al. 2020

Front. Psychiatry

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Brain demyelination is possibly one of the main pathological factors involved in schizophrenia, and targeting on myelination may be a useful strategy for schizophrenia treatment. Quetiapine, a widely used atypical antipsychotic drug for schizophrenia treatment, has been reported to have neuroprotective effects on cerebral myelination in a demyelination animal model. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of quetiapine on the schizophrenia-like behaviors and possible cerebral demyelination induced by MK-801, an N-methyl-Daspartate glutamate receptor antagonist. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). The positive symptom of schizophrenia was measured in a locomotor activity test on day 29, the memory was evaluated by a Y-maze test on day 30, and the sensorimotor gating deficit in mice was measured by prepulse inhibition test on day 31. After the behavioral tests, the protein expression of myelin basic protein (MBP) was measured by Western Blot, and the protein expression of brain-derived neurotrophic factor (BDNF) was measured by ELISA in the frontal cortex of mice. Our results showed quetiapine attenuated schizophrenia-like behaviors including hyperactivity, memory impairment, and sensorimotor gating deficit in the MK-801 mice. In the same time, quetiapine attenuated demyelination, concurrent with attenuated BDNF decrease in the brain of MK-801-injected mice. These results suggest that the beneficial effects of quetiapine on schizophrenia might be partly related to its neuroprotective effect on brain myelin basic protein and its upregulating neuroprotective proteins such as BDNF, and indicate that modulation of cerebral demyelination could be a novel treatment target of schizophrenia.

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Section: Introductionmentioning

confidence: 99%

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Wen³

et al. 2020

Front. Psychiatry

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“…BDNF, a neuroprotective protein, is the most abundant neurotrophin in the brain, and its expression in hippocampus and prefrontal cortex can be affected by prenatal stress [ 19 ]. BDNF regulates neuronal proliferation, survival, and brain development, and represents a potentially relevant gene for schizophrenia [ 20 ]. Reduced expression of cerebral BDNF has been implicated in the pathophysiology of schizophrenia and has been considered to be related to the deficit of PPI, a behavioral endophenotype of schizophrenia [ 7 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

Yang

Liu²,

Yuan³

et al. 2020

NeuroReport

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Increasing evidence supports schizophrenia may be a neurodevelopmental and neurodegenerative disorder. Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to have neuroprotective effects and be effective in treating neurodegenerative disorders including schizophrenia. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of fluoxetine on the sensorimotor gating deficit, a schizophrenia-like behavior in a neurodevelopmental schizophrenic mouse model induced by MK-801, an N -methyl- d -aspartate glutamate receptor antagonist. On postnatal day 7, mouse pups were treated with a total seven subcutaneous daily injections of MK-801 (1 mg/kg/day), followed by intraperitoneal injection of fluoxetine (5 or 10 mg/kg/day) starting on postnatal day 14 in the MK-801-injected mice for 4 weeks. The sensorimotor gating deficit in mice was measured by prepulse inhibition (PPI) behavioral test on postnatal day 43. After the behavioral test, the protein expression of brain-derived neurotrophic factor (BDNF) was measured by western blot or ELISA in the frontal cortex of mice. Our results showed fluoxetine attenuated PPI deficit and the decrease of cerebral BDNF expression in the MK-801-injected mice. These results suggest that fluoxetine can be used to treat sensorimotor gating deficit in a neurodevelopmental mouse model of schizophrenia, and the attenuating effect of fluoxetine on sensorimotor gating deficit may be related to fluoxetine’s neuroprotective effect targeting on the modulation of cerebral BDNF.

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“…BDNF is a neurotrophic factor that plays an important role in neuronal transport, modulation, and plasticity [15]. Some studies also con rmed that changes of BDNF were accompanied by improvement of cognitive functions, such as memory, spatial direction, and learning [16].…”

Section: Discussionmentioning

confidence: 99%

Efficacy and safety of Jie-du-qing-nao granules for first-episode schizophrenics: study protocol for a randomized controlled trial

Ning

Chen

et al. 2020

Preprint

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BackgroundAt present, the focus and difficulty of schizophrenia (SCZ) treatment is to improve cognitive function and negative symptoms. Jie-du-qing-nao granules(JQG) , a traditional Chinese medicine(TCM) prescription , has a good clinical effectiveness in enhancing the cognition and negative symptoms of patients with SCZ. However, its clear effectiveness and safety have not been adequately supported by clinical studies. The main objective of this study is to explore the efficacy and safety of JQG for first-episode schizophrenics.Methods/designThis trial is a prospective, randomized, single-centered, parallel-controlled clinical study with double-blind design. A total of 96 eligible participants will be randomly assigned to either the study group or the control group in a ratio of 1:1. Participants allocated to the study group will receive JQG and aripiprazole, control group will receive placebo and aripiprazole. The treatment course will last 12 weeks, with follow-up every 4 weeks. Outcome measurements include Positive and Negative Syndrome Scale (PANSS), self face test , MATRICS Consensus Cognitive Battery (MCCB), TNFα, IL-6, IL-1β, BDNF, vital signs, complete blood count, liver and kidney function tests, urinalysis, and electrocardiograph. Adverse reactions will be evaluated using the Treatment Emergent Symptom Scale (TESS).DiscussionThis study will provide evidence for the efficacy and safety of JQG as a complementary approach, which can be initiated following with antipsychotics therapy. Trial registration Chinese Clinical Trial Registry, ID: ChiCTR1900028250 . Registered on December 16, 2019, http://www.chictr.org.cn/edit.aspx?pid=41880&htm=4 .

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Brain-derived neurotrophic factor and schizophrenia

Cited by 84 publications

References 98 publications

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

Efficacy and safety of Jie-du-qing-nao granules for first-episode schizophrenics: study protocol for a randomized controlled trial

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