Neuroscience research
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Neuroscience research · Apr 2021
Effects of genome-wide neuroticism-associated variants on five-factor model personality traits in schizophrenia.
Patients with schizophrenia (SCZ) have characteristic personality traits compared with healthy subjects. Genome-wide significant variants for neuroticism have been reported in healthy subjects. However, the associations of these genome-wide neuroticism-associated variants with five-factor personality traits in patients with SCZ are less clear. ⋯ Furthermore, of other personality traits, the genetic variant was significantly associated with higher agreeableness in combined subjects (β = 0.17, p = 9.41×10-3), higher conscientiousness in patients with SCZ (β = 0.21, p = 0.031) and lower conscientiousness in HCs (β = -0.20, p = 0.034), and nominally associated with higher extraversion in patients with SCZ (β = 0.18, p = 0.056) and in combined subjects (β = 0.13, p = 0.051). These outcomes were not affected by clinical variables. We suggest that genome-wide neuroticism-associated variant could be associated with neuroticism as well as other personality traits in schizophrenia.
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Neuroscience research · Sep 2020
miR-101 down-regulates mTOR expression and attenuates neuropathic pain in chronic constriction injury rat models.
We aimed to demonstrate the effects of microRNA (miR)-101 on neuropathic pain and explore the underlying mechanisms. Rat spinal microglia cells were isolated and inflammatory condition was stimulated by 24-h incubation with lipopolysaccharide (LPS). Rats were divided into 4 groups: sham, chronic constriction injury (CCI), CCI + miR-negative control (miR-NC) and CCI + miR-101 mimics. ⋯ In addition, miR-101 downregulated mTOR mRNA and protein expressions in CCI rats. Besides, CCI operation resulted in miR-101 downregulation and mTOR mRNA upregulation in spinal microglia cells in a time-dependent manner. In conclusion, miR-101 had neuropathic pain-attenuating activity through targeting mTOR.
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Neuroscience research · May 2019
Upregulation of Cav3.2 T-type calcium channels in adjacent intact L4 dorsal root ganglion neurons in neuropathic pain rats with L5 spinal nerve ligation.
Besides the injured peripheral dorsal root ganglion (DRG) neurons, the adjacent intact DRG neurons also have important roles in neuropathic pain. Ion channels including Cav3.2 T-type calcium channel in the DRG neurons are important in the development of neuropathic pain. In the present study, we aimed to examine the expression of Cav3.2 T-type calcium channels in the intact DRG neurons in neuropathic pain. ⋯ Western blotting showed that total and membrane protein levels of Cav3.2 in L4 DRG neurons increased, and voltage-dependent patch clamp recordings revealed an increased T-type current density with a curve shift to the left in steady-state activation in the acutely isolated L4 DRG neurons in neuropathic pain rats. Immunofluorescent staining further showed that the membrane expression of Cav3.2 increased in CGRP-, IB4-positive small neurons and NF200-positive large ones. In conclusion, the membrane expression and the function of Cav3.2 T-type calcium channels are increased in the intact L4 DRG neurons in neuropathic pain rats with peripheral nerve injury like SNL.
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Neuroscience research · May 2019
Effects of SC99 on cerebral ischemia-perfusion injury in rats: Selective modulation of microglia polarization to M2 phenotype via inhibiting JAK2-STAT3 pathway.
Inhibition of Janus kinases 2-Signal transducers and activators of transcription3 (JAK2-STAT3) pathway has been shown to exert anti-inflammatory actions. SC99, a novel specific inhibitor targeting JAK2-STAT3 pathway, has been verified to negatively modulate platelet activation and aggregation in vitro. In current study, a middle cerebral artery occlusion and reperfusion (MCAO/R) model was established in Sprague Dawley rats and primary cultured microglia was exposed to oxygen and glucose deprivation (OGD/R) in vitro. ⋯ Correspondingly, SC99 ameliorated neuronal apoptosis and degeneration, neurobehavioral deficits, inflammatory response and brain edema. And SC99 promoted microglia polarization to an anti-inflammatory M2 phenotype. We concluded that SC99 could alleviate brain damage and play an anti-inflammatory action by promoting microglia polarization to an anti-inflammatory phenotype after I/R injury, which provides an emerging and promising alternative to protect the brain against MCAO/R injury in the future investigations.
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Neuroscience research · Apr 2019
ReviewProgression of Alzheimer's disease, tau propagation, and its modifiable risk factors.
The number of patients with Alzheimer's disease (AD) has been increasing exponentially side by side with aging societies worldwide. Symptoms of AD worsen over time due to progressive neurodegeneration, requiring institutional care at the later stage and resulting in a heavy burden on patients, caregivers, and the public-health system. AD neuropathology is characterized by cerebral accumulation and aggregation of amyloid-β (Aβ) and tau proteins. ⋯ AD pathogenesis is multifactorial, and many genetic- and non-genetic factors are known to contribute to Aβ- and tau-related pathology. Recent studies indicate an association between vascular risk factors and AD. Identifying modifiable risk factors for AD and understanding their contributory mechanisms could be key in tackling this devastating disease.