Clinical Neuroscience Research

Slack Channels as Key Regulators of Neuronal Excitability: Implications for Neural Function and the Link to Epilepsy Pathogenesis

2024-10-02T11:31:38+08:00

The Slack channel encoded by the KCNT1 gene is a sodium-activated potassium channel. By regulating the flow of potassium ions, the Slack channel affects the membrane potential and discharge activity of neurons, thus participating in regulating neuronal excitability. Therefore, it plays a crucial role in maintaining the normal function of the nervous system. Consequently, abnormal Slack channel function is closely linked to various neurological diseases, such as epilepsy. Currently, quinidine-based medication therapy and neuroregulatory therapy are key components of the treatment of epilepsy resulting from Slack channel dysfunction. This article aims to outline the fundamental features of the Slack channel while providing a thorough analysis of the main distinctions and possible connections between Slick and Slack channels. Furthermore, this study focuses on the function of controlling the neuronal excitability of Slack channels while delving deeper into the potential correlation between Slack channels and epilepsy and their treatment strategies.

Ameliorative Effect of Hedysarum polybotrys Polysaccharide on Neural Tissue Fibrosis in Diabetic Peripheral Neuropathy Mice and its Mechanisms

2024-10-02T11:31:35+08:00

Objective: This study aimed to investigate the role of Hedysarum polybotrys polysaccharide (HPS) in ameliorating neural tissue fibrosis in diabetic peripheral neuropathy (DPN) mice. Methods: Fifty DPN mice were selected and randomly divided into five groups (n = 10), which were the model group, positive control group (receiving only 4 mg/(kg-d) of α-lipoic acid), high-dose HPS group (200 mg/(kg-d) of HPS was given per day), medium-dose HPS group (100 mg/(kg-d) of HPS was given per day), and low-dose HPS group (50 mg/(kg-d) of HPS given daily). In addition, non-diabetic C57BL/6 wild-type mice were selected as the normal group (n = 10). The expression levels of Keap1 and Nrf2 proteins and their mRNAs in the sciatic nerve tissues of mice in each group were analyzed by Western blot technique and real-time fluorescence quantitative PCR. Results: Compared with the normal group, the expression of Keap1 protein and mRNA was increased, while the expression of Nrf2 protein and mRNA was decreased in the sciatic nerve of mice in the model group (P < 0.05). Compared with the model group, Keap1 protein and mRNA expression decreased, while Nrf2 protein and mRNA expression increased in the control and high and medium dose HPS groups of mice (P < 0.05). Conclusion: HPS may inhibit fibrosis of neural tissue and ameliorate nerve injury in DPN mice by regulating the Keap1/Nrf2 signaling pathway. This effect was associated with enhanced antioxidant capacity, promotion of Nrf2 activation, and increased antioxidant gene expression by HPS. Therefore, HPS has a potential therapeutic value to ameliorate DPN-associated nerve injury.

Research on the Rehabilitation Effect of Repetitive Transcranial Magnetic Stimulation Combined with Cognitive Training on Children with Mental Retardation

2024-10-02T11:31:32+08:00

This study investigated the rehabilitation effect of repetitive transcranial magnetic stimulation (rTMS) combined with cognitive training on children with mental retardation (MR). Through a randomized controlled trial design, 40 children aged 2–6 years with mental retardation were selected as study subjects and randomly divided into two groups: conventional treatment group and rTMS combined with cognitive training treatment group. The results showed that compared with the conventional treatment group, the rTMS combined with cognitive training treatment group exhibited more significant effects in improving children’s cognitive function, social adaptability, and quality of life. This study not only enriched the theoretical basis of rehabilitation treatment for children with mental retardation but also provided strong evidence support for clinical practice.

The Mediating Role of Emotion Regulation Strategies between Symptoms of Attention Deficit Hyperactivity Disorder and Anxiety-Depression Problems in Children

2024-10-02T11:31:30+08:00

The purpose of this study was to investigate the mediating role of emotion regulation strategies of ADHD and anxiety-depression problems in children. Using a cross-sectional research design, this study collected a sample of children with ADHD and assessed their ADHD symptoms, anxiety-depression status, and emotion regulation strategies utilizing standardized tools. The data analysis results showed that emotion regulation strategies played a significant mediating role between ADHD symptoms and anxiety-depression problems, indicating that emotion regulation ability in children with ADHD may be an important factor affecting their anxiety and depression. This study not only provides a new perspective for understanding the emotional and behavioral problems of children with ADHD but also offers empirical evidence for developing targeted intervention measures. In the future, training in emotion regulation strategies is expected to become an important part of interventions for children with ADHD.

Effect of Blood Glucose Gap on Post-stroke Cognitive Impairment in Acute Ischemic Stroke Patients

2024-10-02T11:31:28+08:00

Objective: To analyze the effect of the blood glucose gap on post-stroke cognitive impairment in acute ischemic stroke patients. Methods: 300 stroke patients admitted to the hospital between December 2021 and December 2022 were selected and divided into three groups according to the value of blood glucose gap: the group with no elevation of blood glucose gap (n = 124), the group with mild elevation of blood glucose gap (n = 97), and the group with elevated blood glucose gap (n = 79). The same treatment regimen was applied to these three groups and cognitive function was assessed using MMSE and MoCA at 3, 6, and 12 months after discharge. Results: The NIHSS and MoCA scores of the patients in the group with elevated blood glucose gap were significantly higher than those in the mildly elevated group and the non-elevated group at 3, 6, and 12 months after discharge, and the MMSE and MoCA scores of the patients in the group with mildly elevated blood glucose gap were significantly higher than those in the non-elevated group at 3, 6, and 12 months after discharge, and there were statistically significant differences between all the groups (P < 0.05). Conclusion: Patients with an elevated glycemic gap in acute ischemic stroke showed more pronounced cognitive impairment than those with no elevated glycemic deficit, and the severity of cognitive impairment increased with the degree of glycemic deficit.

Advancements in the Study of Clinical Features and Molecular Functions in Heterogeneous TAF1-associated Clinical Phenotypes

2024-10-02T11:31:25+08:00

Purpose of review: TATA-binding protein (TBP)-associated factor 1 (TAF1) encodes the largest component of the transcription factor IID (TFIID) complex, which binds to core promoters and serves as a scaffold for assembly of the RNA polymerase II transcription complex. Variants in TAF1 are associated with X-linked dystonia-parkinsonism (XDP) and X-linked syndromic mental retardation-33 (MRXS33). This review provides a concise summary of the genetic and clinicopathological features of TAF1 variants related to phenotype. Recent findings: XDP is an adult-onset X-linked progressive neurodegenerative disorder presenting dystonia and parkinsonism and caused by a SINE-VNTR-Alu (SVA)-type retrotransposon within TAF1. TAF1/MRXS33 intellectual disability syndrome is characterized by global developmental delay, intellectual disability, facial dysmorphia, generalized hypotonia, and neurological abnormalities due to the missense variants in TAF1. Various symptoms of TAF1 missense mutations may be related to mutations in different functional regions of the protein. The clinical manifestations of XDP and MRXS33, both caused by variants of TAF1, present prominent heterogeneity, which could be influenced by whether the TAF1 mutation is located in the coding region, the time when TAF1 expression decreases, and the effect on downstream gene expression. Summary: TAF1 is linked to many different phenotypes because of its variable regulation of coding and noncoding elements, which makes its mechanistic roles in disease challenging to interpret. However, it is important to note that strategies to correct TAF1 splicing could provide therapeutic benefits in different diseases.

Aquaporin-4 IgG Antibody Detection in Neuromyelitis Optic Spectrum Disorder

2024-10-02T11:31:22+08:00

Objective: To develop a sensitive and reliable diagnostic approach for optic neuromyelitis (ONM), an overexpressing cell line capable of detecting aquaporin 4 (AQP4) antibodies was established. Subsequently, immunofluorescence was employed to detect AQP4 antibodies in serum and cerebrospinal fluid (CSF) samples from patients. Additionally, the clinical utility of AQP4 antibodies in the detection of ONM patients was analyzed. Methods: An aquaporin 4 expression plasmid was constructed and transfected into cell lines. Subsequently, indirect immunofluorescence was utilized to detect anti-AQP4 antibodies in serum and cerebrospinal fluid samples. Results: The indirect immunofluorescence detection system exhibited high sensitivity in the detection of 2241 clinical samples, with a positive rate of 16.8%. The positive proportion was in line with epidemiological data, and the positive situation was consistent with clinical symptoms. Conclusion: The engineered cell line exhibits superior detection performance for identifying antibodies present in serum and cerebrospinal fluid samples. The capability to detect anti-aquaporin 4 antibodies is pivotal for improving the efficiency of screening and diagnosing neuromyelitis optica, thereby possessing considerable potential for clinical application.

High Ambient Temperatures Increase Outpatient Visits for Sleep Disorders in Hefei City, China

2024-10-02T11:31:41+08:00

Objective: To analyze the impact of ambient temperature on the quantity of outpatient clinic visits for sleep disorders. Methods: Using data from sleep disorder outpatient visits in a large tertiary hospital in Hefei City, a distributional lag nonlinear model combined with a generalized Poisson regression model was used to analyze the relationship between ambient temperature and the number of outpatient visits for sleep disorders. Results: Ambient temperatures above 17.2℃ were found to be connected with a higher prevalence of sleep disorders visits, and that this relationship was most significant on day 8, which lasted for 7 days. For the single-day lagged impact, the maximum relative risk (RR) for moderate heat (75th percentile) was 1.077 (95% CI: 1.015–1.143). The cumulative lag effect was substantially greater than the single-day lag effect, with a maximum relative risk (RR) of 2.609 (95% CI: 1.306–5.212). The longest lag time was 14 days. The RR was similarly greater in women and those over 40. Outpatient visits for men with sleep disorders were not affected by ambient temperature in a statistically significant way. Conclusion: High ambient temperature raises the risk that patients will visit an outpatient facility and serves as a risk factor for sleep disorders. Patients who were 40 years of age or older and women were at vulnerability.