International Journal of Neuroscience最新文献

Empagliflozin, a sodium-glucose co-transporter 2 (SGLT2) inhibitor, has recently reported to prevent the depression in chronic animal model. The present study aimed to explore the antidepressant potential of empagliflozin using a neuroinflammation-mediated depression involving the olfactory bulbectomy (OBX) model in diabetic rats. A low dose of streptozotocin was injected to induce diabetes in all group of animals. Following the confirmation of hyperglycemia, OBX surgery was performed. Post-surgery, the drug treatments were administered orally for 14 consecutive days. The study evaluated the effects of daily oral administration of empagliflozin at doses of 5 and 10 mg/kg, alongside metformin (200 mg/kg) and clomipramine (50 mg/kg), on OBX-induced behavioral depression in rats. Separate sham and vehicle control groups were also maintained. Behavioral parameters in open field, forced swim test, elevated plus maze and splash test were recorded on 28^th day. Results showed that empagliflozin, at the higher dose, significantly enhanced behavioral outcomes, evidenced by increased distance travelled, greater open arm entries, and reduced immobility, alongside a notable reduction in grooming time. Moreover, empagliflozin significantly restored the antioxidants level specifically Glutathione (GSH) and Catalase (CAT) in OBX insulted rat brain and decreased Lipid peroxidase (LPO). Notably, molecular docking study demonstrated a good binding affinity of empagliflozin for Brain-Derived Neurotrophic Factor (BDNF), suggesting that its antidepressant effects may be mediated through the modulation of the BDNF pathway. These findings support the potential therapeutic application of empagliflozin for depression, particularly in cases associated with neuroinflammation and oxidative stress.

Background: Chemotherapy-induced peripheral neuropathy not only affects the tolerability of chemotherapy, but also causes intolerable and prolonged neuropathic pain in cancer patients. Currently, duloxetine is the only drug used to treat chemotherapy-induced peripheral neuropathy. However, the clinical use of this drug still faces several challenges. Therefore, we focused on traditional Chinese medicine to find an effective and safe alternative medicine. Huangqi Guizhi Wuwu Decoction is a traditional Chinese medicine that has been clinically used for treating nerve pain for thousands of years. This study aimed to investigate the neuroprotective effect of Huangqi Guizhi Wuwu Decoction on cisplatin-induced nerve injury in PC12 cells and to elucidate its potential mechanism of action.

Methods: Huangqi Guizhi Wuwu Decoction-containing serum and blank serum were prepared from a rat model. The protective effects of Huangqi Guizhi Wuwu Decoction on cisplatin (10 µmol/L)-induced PC12 cell injury were assessed by a Cell Counting Kit-8 assay. RNA expression in Huangqi Guizhi Wuwu Decoction-protected PC12 cells was analyzed using RNA-seq, and subsequently, differentially expressed genes were further analyzed using Gene Ontology and Gene Set Enrichment Analysis.

Results: The Cell Counting Kit-8 results showed that pretreatment of PC12 cells with Huangqi Guizhi Wuwu Decoction-containing serum (5%, 10%, 15%) significantly increased cells' viability to 10 µmol/L cisplatin-induced cell death. RNA-seq analysis revealed 843 differentially expressed genes in the chemotherapy-induced peripheral neuropathy group and 249 in the Huangqi Guizhi Wuwu Decoction group. The gene set enrichment analysis results in this study suggest that Huangqi Guizhi Wuwu Decoction may treat chemotherapy-induced peripheral neuropathy by enhancing axon guidance.

Conclusions: This study provides valuable evidence for using Huangqi Guizhi Wuwu Decoction in treating chemotherapy-induced peripheral neuropathy, partially achieved by improving axon guidance pathways.

Background: Autoimmune encephalitis (AE) is a group of autoimmune diseases targeting the central nervous system, characterized by severe clinical symptoms and substantial consumption of medical resources. Neuroinflammation plays a crucial role in disease progression, and detecting inflammatory responses can provide insights into disease status and disease severity. The systemic immune-inflammation index (SII), a novel marker of inflammatory status, has been rarely studied in AE.

Methods: Retrospective analysis of data from AE patients admitted to the First Affiliated Hospital of Zhengzhou University between January 2019 and September 2023 was conducted. Univariate analysis and logistic regression were used to assess the association between SII and patient severity. Nomograms for predicting AE severity were established, and receiver operating characteristic (ROC) curves, concordance index (C-index), calibration curves, and decision curve analysis were employed to evaluate predictive accuracy. Additionally, the Clinical Assessment Scale in Autoimmune Encephalitis (CASE) score was used to assess patient severity.

Results: This study enrolled 157 patients, of whom 57 were classified as severe according to the CASE score. SII, cerebrospinal fluid (CSF) cell counts, disturbance of consciousness, and behavioural abnormalities independently associated with the occurrence of severe cases. The C-index of the nomograms was 0.87, indicating strong association with disease severity, as supported by the calibration. Additionally, SII levels were highest within seven days of onset and decreased after one month. In subgroup analyses of different antibodies, SII also associations with severe cases in NMDAR encephalitis.

Conclusions: Higher SII levels are associated with an increased likelihood of developing severe AE, peaking within 7 days of disease onset and decreasing thereafter, potentially offering a prognostic marker to assess disease progression early in its course.

Background: Post coronavirus disease 2019 (COVID-19) pandemic, the widespread emergence and persistence of brain fog has led to a decline in people's productivity and quality of life. However, the clinical characteristics of COVID-19-associated brain fog are unclear, and standardized assessments are lacking. This study aims to develop a scale for brain fog assessment and support clinical practice and research.

Methods: The 17-item Brain Fog Assessment (BFA) scale was developed using a standardized methodology, including literature review, focus group discussions (FGDs), expert evaluation, and psychometric validation. Eighteen potential items were generated following the literature review. These items were subsequently refined during FGDs, which included input from patients, caregivers, and multidisciplinary experts in neurology, cognitive neuroscience, and psychology. After thorough deliberation and expert evaluation, the item pool was finalized into a 17-item scale. We recruited 1,325 patients recovered from COVID-19 from Chinese communities. Psychometric properties were assessed by reliability and validity analysis.

Results: Exploratory factor analysis of the BFA scale revealed a three-factor mode comprising 'cognitive decline' (nine items), 'confusion - disorientation' (five items), and 'fatigue' (three items). The internal consistency of each factor was strong (Cronbach's α: 0.82-0.92). Confirmatory factor analysis showed that the model fit, convergent validity, and discriminant validity of the scale were satisfactory. The test-retest reliability was strong (intraclass correlation coefficient = 0.84). Criterion-related validity analysis showed a strong correlation to the Wood Mental Fatigue Inventory (r = 0.70, p < 0.001). Individuals with a higher BFA score tended to score lower on the Montreal Cognitive Assessment (r = -0.23, p = 0.015).

Conclusions: We established a novel BFA scale to quantify multiple clinical aspects of COVID-19-associated brain fog. Using the BFA scale, fatigue and declining performance in memory, attention, and thought were identified as the main symptoms of COVID-19-associated brain fog. This scale has potential implications for disease monitoring and therapy development for individuals with COVID-19-associated brain fog.

Objectives: Strong evidence suggests the occurrence of cerebral microbleeds (CMBs) in 5-13% of stroke patients within the first week after stroke onset. The aim of this work was to study risk factors associated with occurrence of CMBs in patients with stroke who received intravenous thrombolysis, and to clarify their impact on the clinical outcome.

Methods: This prospective observational study was conducted on 61 acute ischemic stroke patients eligible for treatment with recombinant tissue plasminogen activator (rt-PA). Assessment of stroke-related neurologic deficit was done using National Institute of Health Stroke Scale (NIHSS). Assessment of stroke related disability after 3 months from stroke onset was done using Modified Rankin Scale (mRS). CMBs were detected by T2*-weighed gradient-recalled echo (T2*-GRE) and susceptibility-weighted imaging (SWI) magnetic resonance imaging (MRI) sequences.

Results: There was a statistically significant impact of age, mean arterial pressure (MAP) at stroke onset, history of hypertension (HTN), and white matter changes assessed by Fazekas scale on the occurrence of CMBs in the included stroke patients (P-value= 0.002, <0.001, <0.001, 0.008 respectively). There was no statistically significant difference between patients with favorable and those with unfavorable outcome regarding the total number of CMBs (P-value =0.542). There was also no statistically significant difference between patients who developed complications from rt-PA and those who didn't develop regarding the total number of CMBs (P-value =0.186).

Conclusion: Cerebral microbleeds are more likely to occur in older stroke patients and in those who had high MAP at stroke onset, history of HTN, and white matter changes.

Objective: To analyze the efficacy of early prone position ventilation in the treatment of severe hypoxemia after surgery for acute type A aortic dissection (TAAD).

Methods: The patients were divided into a control group and a treatment group. Parameters assessed included blood gas analysis indicators [arterial oxygen partial pressure (PaO2).

Results: (1) Blood gas analysis: Before treatment, there was no significant difference in PaO2, SpO2, and OI levels between the two groups; after treatment, the PaO2, SpO2, and OI levels in both groups significantly increased compared to pre-treatment, with a more pronounced improvement in the treatment group than in the control group (p < 0.05). (2) Hemodynamics: Before treatment, there was no significant difference in MAP and HR levels between the two groups; after treatment, the MAP levels increased significantly in both groups compared to pre-treatment, while HR levels decreased significantly, with no significant difference between the groups. (3) Prognosis recovery: MV time, ICU stay, and total hospital stay were significantly lower in the treatment group than in the control group; the 30-day mortality rate was 14.58% in the control group and 12.50% in the treatment group, with no significant difference in 30-day mortality rate between the groups.

Conclusion: Early prone position ventilation has shown promising application in the treatment of severe hypoxemia after TAAD surgery. Compared to traditional supine position ventilation, the use of early prone position ventilation can further improve blood gas analysis indicators in patients, and shorten MV time, ICU stay, and total hospital stay, thereby accelerating patient recovery.

Objective: To observe the clinical efficacy of calcipotriol combined with AYJ(An Yi Jia) sodium alginate repair dressing in the treatment of psoriasis vulgaris (PV) and its effect on patients' neurological function.

Methods: A retrospective analysis was conducted on the clinical data of 103 patients with PV admitted to our hospital from January 2022 to January 2024. All patients met the inclusion and exclusion criteria. According to the treatment interventions received by the patients, they were divided into control group (n = 51, receiving calcipotriol monotherapy) and observation group (n = 52, receiving calcipotriol combined with AYJ sodium alginate repair dressing). The clinical treatment effects, severity of the disease (PSSI score), levels of T lymphocyte subsets (CD4+, CD8+), serum nerve growth factor (NGF), inflammatory factors [interferon-gamma (IFN-γ), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-α)], and adverse reactions were compared between the two groups.

Results: ① Clinical treatment effects: The total effective rate in the observation group was higher than that in the control group (p < 0.05). ② Severity of the disease: The PASI scores of both groups gradually decreased with prolonged treatment time, and the observation group showed a greater magnitude of change (p < 0.05). ③ T lymphocyte subset cells and serum nerve growth factor: The levels of CD4+ were increased after treatment in both groups, while CD8+ and NGF levels were decreased compared to before treatment, with a greater magnitude of change in the observation group (p < 0.05). ④ Inflammatory factors: The levels of IFN-γ, IL-8, and TNF-α were decreased after treatment in both groups, with a greater magnitude of change in the observation group (p < 0.05). ⑤ Adverse reactions: There was no significant difference in the incidence of adverse reactions between the two groups (p > 0.05).

Conclusion: Calcipotriol combined with AYJ sodium alginate repair dressing has ideal therapeutic effects in the treatment of PV. Compared with calcipotriol alone, the combined application of AYJ sodium alginate repair dressing can further improve patient efficacy, improve immune and neurological function, alleviate patient inflammatory responses, and does not increase the risk of adverse reactions in patients.

Transcranial direct current stimulation (tDCS) has been used with increasing frequency as a therapeutic tool to alleviate clinical symptoms of obsessive compulsive-disorder (OCD). However, little is known about the effects of tDCS on neurocognitive functioning among OCD patients. The aim of this review was to provide a comprehensive overview of the literature examining the effects of tDCS on specific neurocognitive functions in OCD. A literature search following PRISMA guidelines was conducted on the following databases: PubMed, PsycINFO, Embase, the Cochrane Central Register of Controlled Trials (CENTRAL), the Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science. The search yielded 4 results: one randomized, sham-controlled study (20 patients), one randomized, controlled, partial crossover trial (12 patients), one open-label study (5 patients), and one randomized, double-blind, sham-controlled, parallel-group trial (37 patients). A total of 51 patients received active tDCS with some diversity in electrode montages targeting the dorsolateral prefrontal cortex, the pre-supplementary motor area, or the orbitofrontal cortex. tDCS was associated with improved decision-making in study 1, enhanced attentional monitoring and response inhibition in study 2, improved executive and inhibitory control in study 3, and reduced attentional bias and improved response inhibition and working memory in study 4. Limitations of this review include its small sample, the absence of a sham group in half of the studies, and the heterogeneity in tDCS parameters. These preliminary results highlight the need for future testing in randomized, sham-controlled trials to examine whether and how tDCS induces relevant cognitive benefits in OCD.

Aim: Neuropathic pain occurs commonly after stroke and represents a major source of disability for affected patients. This study aims to develop an accurate and computationally efficient framework for multi-level neuropathic pain detection using electroencephalography signals.

Methods: A Quantum-Inspired Pyramid Depthwise Separable Residual Network is proposed, which integrates three innovations: a depthwise separable Residual Network to reduce computational complexity, a pyramid attention mechanism to capture multi-scale patterns, and a quantum-inspired transformation layer to model complex nonlinear dependencies among Electroencephalogram features.

Results: Experiments conducted on benchmark electroencephalography datasets confirm that the proposed model gains a accuracy of 99.65%, with a recall of 98.00%.

Conclusion: The proposed model provides a reliable solution for objective neuropathic pain detection in post-stroke patients. The framework demonstrates potential for integration into intelligent clinical decision-support and brain-computer interface-based rehabilitation systems.

Background: Ischemic stroke, a major cause of disability and death, results from blocked cerebral blood flow, causing neuronal damage. Limited treatments necessitate research into molecular mechanisms for targeted therapies.

Methods: In this study, we analyzed transcriptomic data from the Gene Expression Omnibus (GEO) database (GSE36010), focusing on gene expression changes in the core region of the brain 24 h post-stroke induction. Enrichment analysis of differentially expressed genes (DEGs) was conducted using Enrichr, exploring Gene Ontology (GO) terms and Reactome pathways. A protein-protein interaction network (PPIN) was constructed using STRING, and hub genes were identified through the CytoHubba plugin in Cytoscape. Network clustering analysis was performed using the iterative partition-based clustering algorithm (IPCA) in CytoCluster. Promoter motif analysis of hub genes was conducted using TomTom and GO for motifs (GOMO), while DrugBank analysis was used to identify potential therapeutic compounds targeting the identified hub proteins.A total of 150 DEGs were identified in the core region of ischemic stroke, with significant enrichment in pathways related to inflammation, oxidative stress, apoptosis and vascular remodeling. Key hub genes like cluster of differentiation 68 (Cd68), chemokine (C-C motif) ligand 3 (Ccl3), transforming growth factor beta 1 (Tgfb1), cluster of differentiation 44 (Cd44), Lgals3, topoisomerase II alpha (Top2a), lipocalin 2 (Lcn2), chemokine (C-C motif) ligand 4 (Ccl4), Ckap2 and cell division cycle associated 2 (Cdca2) were found to play critical roles in neuronal survival, inflammation and vascular integrity. Additionally, drug analysis highlighted several FDA-approved drugs that could be repurposed for stroke therapy, emphasizing the potential therapeutic candidates targeting these hub proteins.

Conclusion: This study analyzes ischemic stroke, identifying key pathways and drug targets, potentially aiding in developing targeted therapies to reduce damage and improve outcomes for stroke patients.