Publications by authors named "Yuan-Jian Yang"

Objective: Auditory hallucinations are the most frequently occurring psychotic symptom in schizophrenia. Continuous theta burst stimulation (cTBS) has been used as an adjuvant treatment for auditory hallucinations. This meta-analysis focused on randomized controlled clinical trials (RCTs) to assess the efficacy of adjuvant cTBS on auditory hallucinations in schizophrenia.

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Objective: Accumulating evidence has indicated that neurodevelopmental defects may underlie the pathophysiology of bipolar disorder (BD). Insulin-like growth factors (IGFs) are a family of neurotrophic factors that are essential for the survival and development of neurons. The present study aims to investigate whether IGF-2 signaling is implicated in the pathophysiological processes of BD.

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Depression is a high-incidence mental illness that seriously affects human health. AQP4 has been reported to be closely associated with depression, while the underlying mechanism is still unclear. This work aimed to investigate the functional role of AQP4 in depression.

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Klotho is a life extension factor that has the ability to regulate the function of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs), whose dysfunction in the nucleus accumbens (NAc) underlies critical aspects of the pathophysiology of major depression. Here, we study the functional relevance of klotho in the pathogenesis of depression. A chronic social defeat stress paradigm, in which mice are categorized as either susceptible or unsusceptible based on their performance in a social interaction test, was used in this study.

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Accumulating evidence has suggested a dysfunction of synaptic plasticity in the pathophysiology of depression. Hydrogen sulfide (HS), an endogenous gasotransmitter that regulates synaptic plasticity, has been demonstrated to contribute to depressive-like behaviors in rodents. The current study investigated the relationship between plasma HS levels and the depressive symptoms in patients with depression.

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Cognitive deficits are the core feature of schizophrenia and effective treatment strategies are still missing. Previous studies have reported that fisetin promotes long-term potentiation (LTP) and cognitive function in normal rodents and other model animals of neurological diseases. The aim of this study was to assess the effect of fisetin on synaptic plasticity and cognitive deficits caused by a brief disruption of N-methyl-D-aspartate receptors (NMDARs) with dizocilpine (MK-801) during early development in rats.

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Article Synopsis
  • Schizophrenia is associated with abnormal neurodevelopment, and while growth differentiation factor 11 (GDF-11) might play a role, direct evidence linking it to the disorder is lacking.
  • This study involved 87 schizophrenia patients and 76 healthy controls, using the Positive and Negative Syndrome Scale (PANSS) and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to evaluate symptoms and cognitive function, respectively.
  • The findings indicated that GDF-11 levels were significantly lower in schizophrenia patients compared to controls, with negative correlations to symptom severity and positive correlations to specific cognitive functions, suggesting GDF-11 may contribute to both psychopathology and cognitive impairments in schizophrenia.
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The article "Changes of Serum Insulin-like Growth Factor-2 Response to Negative Symptom Improvements in Schizophrenia Patients Treated with Atypical Antipsychotics", written by Xue-lin CHAO, Shu-zhen JIANG, Jian-wen XIONG, Jin-qiong ZHAN, Bo WEI, Chun-nuan CHEN, Yuan-jian YANG was originally published electronically on the publisher's internet portal on June 2020 without open access. With the author(s)' decision to opt for Open Choice, the copyright of the article is changed to © The Author(s) 2020 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License (https://creativecommons.

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Fear-related anxiety disorders, such as social phobia and post-traumatic stress disorder, are partly explained by an uncontrollable state of fear. An emerging literature suggests dopamine receptor-1 (D receptor) in the amygdala is involved in the regulation of fear memory. An early study has reported that amygdaloid D receptor (DR) is not coupled to the classic cAMP-dependent signal transduction.

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Microglia polarization is associated with the pathogenesis of depression. A previous study shows that long non-coding RNA uc.80- is down-regulated in the hippocampus of depressed rats.

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Accumulating evidence suggests that a disruption of early brain development, in which insulin-like growth factor-2 (IGF-2) has a crucial role, may underlie the pathophysiology of schizophrenia. Our previous study has shown that decreased serum IGF-2 was correlated with the severity of psychopathology in patients with schizophrenia. Here we conducted a prospective observation trial to investigate the effects of atypical antipsychotics on serum IGF-2 level and its relationship with clinical improvements in schizophrenia patients.

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Cognitive impairments are a core feature of schizophrenia. Klotho is an anti-aging protein with demonstrated cognitive-enhancing effects on the brain. The purpose of this study was to investigate the differences in levels of plasma klotho between patients with schizophrenia and healthy controls, as well as the relationship between klotho level and cognitive function in patients.

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Background: Schizophrenia is linked with abnormal brain neurodevelopment, on which IGF-2 (insulin-like growth factor-2) has a great impact. The purpose of this study was to assess the levels of serum IGF-2 and its binding proteins IGFBP-3 and IGFBP-7 in schizophrenia patients and the associations of these proteins with schizophrenia psychopathology and cognitive deficits.

Methods: Thirty-two schizophrenia patients and 30 healthy controls were recruited.

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Accumulating evidence has shown that insulin-like growth factors (IGFs) are implicated in schizophrenia. Altered serum levels of IGF-1 have been found in schizophrenia patients and are associated with psychopathological symptoms. However, whether there is a relationship between IGF-1 and cognitive impairment in schizophrenia remains unknown.

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The aim of this paper was to investigate the effect of total saponins from Panax japonicus( SPJ) on cognitive decline of natural aging rats and its mechanism. Thirty male SD rats of eighteen month old were randomly divided into three groups: aged group,10 mg·kg~(-1) SPJ-treated group and 30 mg·kg~(-1) SPJ-treated group. The SPJ-treated groups were given SPJ at the dosages of 10 mg·kg~(-1) and 30 mg·kg~(-1),respectively,from the age of 18 to 24 months.

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Background: It is well known that aripiprazole co-treatment effectively reduces antipsychotic-induced hyperprolactinemia. However, the effectiveness of aripiprazole to treat high prolactin levels induced by antidepressant drugs with serotoninergic activity, such as duloxetine, remains unknown.

Case Presentation: An 18-year-old female diagnosed with major depressive disorder (MDD) was treated with 100 mg sertraline once daily.

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Cognitive deficits represent a core feature of schizophrenia. Previous studies have demonstrated that plasma asymmetric dimethylarginine (ADMA) was increased in patients with schizophrenia and correlated with cognitive impairments. Atypical antipsychotics can produce cognitive benefits in schizophrenia patients.

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As an endogenous neuromodulator, hydrogen sulfide (HS) exerts multiple biological effects in the brain. Previous studies have shown that HS is involved in the regulation of neural synaptic plasticity and cognition in healthy rodents. It is well known that there is a progressive decline of cognitive function that occurs with increased age.

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Objective: Aberrant N-methyl-D-aspartate receptor (NMDAR) function has been implicated in the pathophysiology of schizophrenia. Hydrogen sulfide (HS) is an endogenous gasotransmitter that regulates NMDAR function. The current study investigated the relationship between plasma HS levels and both psychopathological and cognitive symptoms in schizophrenia.

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Background: Epilepsy is a common neurological disorder and is not well controlled by available antiepileptic drugs (AEDs). Inflammation is considered to be a critical factor in the pathophysiology of epilepsy. Sinomenine (SN), a bioactive alkaloid with anti-inflammatory effect, exerts neuroprotective activity in many nervous system diseases.

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Neuroinflammation is recognized as an important pathogenic factor for aging and related cognitive disorders. Mitogen-activated protein kinase and nuclear factor kappa B signaling pathways may mediate neuroinflammation. Saponins from Panax japonicus are the most abundant and bioactive members in rhizomes of Panax japonicus, and show anti-inflammatory activity.

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Hydrogen sulfide (HS) is an endogenous gaseous molecule that functions as a neuromodulator in the brain. We previously reported that HS regulated amygdalar synaptic plasticity and cued fear memory in rats. However, whether endogenous HS is required for amygdalar long-term potentiation (LTP) induction and cued fear memory formation remains unclear.

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Cognitive deficits are a core feature of schizophrenia. Previous studies have shown that plasma asymmetric dimethylarginine (ADMA), an endogenous inhibitor of the nitric oxide synthase, was increased in patients with schizophrenia. This study aimed to investigate the association of ADMA with cognitive deficits in schizophrenia.

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Alzheimer's disease (AD) is the most common type of clinical dementia. Previous studies have demonstrated that hydrogen sulfide (H2S) is implicated with the pathology of AD, and exogenous H2S attenuates spatial memory impairments in AD animal models. However, the molecular mechanism by which H2S improves cognition in AD has not been fully explored.

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