Neurology Research International最新文献

Cerebrovascular accident is a neurological disease, characterised by acute onset that lasts for more than 24 h, leading to motor, sensory and cognitive impairments or even death. High-intensity interval training is a type of aerobic training that presents an increase of the > 80% of maximum heart rate, aiming to improve VO₂ peak, leading to improvements in various health-related parameters. The purpose of this study was to examine the effectiveness of high-intensity interval training on aerobic and functional capacity for poststroke survivors. Two investigators searched the electronic databases MEDLINE/PUBMED, Cochrane Controlled Trials Register and EBSCO, until August 2024. In this review, 11 studies met the eligible criteria and were included. The statistical analysis was conducted by pooling the mean, standard deviation, and 95% confidence intervals. For the establishment of meta-analysis, the heterogeneity statistical index I ² was used. From the 11 included studies, 458 stroke survivors were extracted. HIIT yield improvements were observed in VO₂ peak (p value = 0.001, 95% CI: 1.72-4.06), 6MWT (p value < 0.001, 95% CI = 38.55-149.41), 10MWT (p value < 0.01, 95% CI = 0.20-0.36), BBS (p value < 0.01, 95% CI = 3.43-7.51), EQ-5D (p value = 0.001, 95% CI = 3.67-15.13), and cognition (p value = 0.009, 95% CI = 0.41-2.89). No significant difference was presented for HR (p value = 0.58, 95% CI = -11.82-21.10), TUG (p value = 0.055, 95% CI = -2.25 to 0.02) and step count (p value = 0.71, 95% CI = -1479-2163). High-intensity interval training is a safe rehabilitation method affecting positively the aerobic capacity and the majority of motor function of stroke survivors.

Objective: To investigate the association between lipid profiles and disease severity/cranial nerve involvement in Guillain-Barré syndrome (GBS), providing evidence for early clinical intervention. Methods: This retrospective study enrolled 182 GBS patients (148 males and 34 females) admitted to the First Affiliated Hospital of Shihezi University from December 2019 to April 2024. Patients were stratified into mild (Hughes Functional Disability Scale [HFDS] 1-3) and severe (HFDS 4-6) groups. Multivariate logistic regression (adjusted for age, sex, and antecedent infections) was used to analyze independent associations of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein A (ApoA) with disease severity and cranial nerve involvement. ROC curve analysis determined predictive thresholds. Results: Disease severity: each 1 mmol/L increase in LDL elevated severe disease risk by 2.5-fold (OR = 2.503, p=0.009) and each 0.1 g/L decrease in ApoA reduced severe disease risk by 99.6% (OR = 0.004, p < 0.001). Cranial nerve involvement: LDL ≥ 2.355 mmol/L significantly increased cranial nerve involvement risk (OR = 1.925, p=0.018). Predictive thresholds: LDL ≥ 2.215 mmol/L optimally predicted severe disease and ApoA ≤ 1.071 g/L indicated higher probability of mild disease. Conclusion: Elevated LDL and reduced ApoA are independent risk factors for GBS progression and cranial nerve involvement. Combined detection may aid early identification of high-risk patients. Dyslipidemia likely exacerbates GBS pathology through neuroinflammatory mechanisms, suggesting targeted lipid regulation as a potential therapeutic strategy.

Introduction: Due to anti-inflammatory, antioxidant, immune-modulating, and antiaging properties of astaxanthin, it has been used to treat spinal cord injuries (SCIs). In this meta-analysis study, the effects of astaxanthin on SCI in animal models were investigated. Method: Scopus, PubMed, Web of Science, and Google Scholar databases were searched based on keywords related to astaxanthin and SCI. The primary screening of articles based on the title and abstract and the secondary screening based on the full text of the articles according to inclusion and exclusion criteria were performed. After extracting the data, statistical analysis was done using STATA software. A standardized mean difference (SMD) was used to analyze the results of the reported studies. Subgroup analysis and quality control of articles was also performed. Result: The overall results showed that astaxanthin has a strong effect (SMD = 3.34; 95% CI: 1.90 to 4.78; p < 0.001) on improving motor function after SCI especially when administered in multiple doses over consecutive days. Astaxanthin has a strong effect on reducing lipid peroxidation and increasing antioxidants. Treatment with astaxanthin increased the number of spinal cord neurons and spared white matter. Conclusion: Astaxanthin has the potential to be used as an adjuvant in improving motor behavior, and it is suggested to conduct clinical studies on it.

Background: Parkinson's disease is a neurodegenerative disorder that affects balance and increases the risk of falling by compromising vestibular signal processing. Objectives: This study aims to assess the impact of vestibular-oriented balance training on postural control and fall risk among people in the middle stages of PD. Methods: Forty middle-stage individuals with PD were assigned to the vestibular-oriented balance training (study group) or the traditional balance training (control group). Outcome measures including Functional Gait Assessment (FGA) and modified Clinical Test of Sensory Interaction on Balance (mCTSIB) using the Biodex Balance System were measured before, immediately after and 4 weeks after treatment. Results: There was a significant group interaction by time for all outcome measures (p < 0.001). The results showed that the difference in the FGA and mCTSIB scores from baseline was significant between the two groups at all time points (p < 0.001). The study group showed significant sustained improvements in the FGA score overtime, while the control group had a significant improvement at Week 8 but that did not last to Week 12. In mCTSIB, the study group improved significantly in all test conditions (p < 0.001), while the control group showed significant improvement only in Conditions 1 and 2, without lasting effects at Week 12 (p > 0.05). Conclusions: The findings indicate that the implementation of vestibular-oriented balance training during the middle stage of PD might have a notable and lasting impact on both postural control and the risk of falls.

Background: Abnormal elevation of transforming growth factor-beta (TGF-β) has been observed among Alzheimer's disease (AD) patients. This may be due to microglia-mediated release of proinflammatory cytokines, which promote neuroinflammation and neuronal apoptosis. Silencing of TGFBR1, a gene encoding TGF-β receptor type I (TGF-βR1), has resulted in neuronal survival from amyloid-beta (Aβ)-induced neurotoxicity. Therefore, the present study investigated the neuroprotective effect of TGF-βR1 inhibitors (RepSox, Galunisertib, and Vactosertib) against Aβ-induced direct neurotoxicity and microglia-mediated neuroinflammation. Methods: The neuroprotective effect of TGF-βR1 inhibitors against Aβ-induced direct neurotoxicity and microglia-mediated neuroinflammation were investigated using the RealTime-Glo™ MT Cell Viability Assay. The inhibitory effect of TGF-βR1 inhibitors on Aβ-induced microglia-mediated production of proinflammatory cytokines (TNF-α and IL-1β) was determined using enzyme-linked immunosorbent assay (ELISA). Results: TGF-βR1 inhibitors (RepSox, Galunisertib, and Vactosertib) at the tested concentrations (6.25-150 nM) showed no significant cytotoxicity effects on SH-SY5Y and BV-2 cells. Moreover, treatments with these inhibitors exhibited neuroprotection on SH-SY5Y cells against Aβ-induced direct neurotoxicity. The trend of cell viability after 24 h treatment also supports the microscopic images of the cells' morphology. Furthermore, pretreatment with these inhibitors conferred indirect neuroprotective effect against Aβ-induced microglia-mediated neuroinflammation by attenuating the production of proinflammatory cytokines (TNF-α and IL-1β). Conclusion: The inhibition of the TGF-β signaling pathway in neuronal and microglia cells by TGF-βR1 inhibitors resulted in neuroprotection against Aβ-induced direct neurotoxicity and microglia-mediated neuroinflammation. Hence, targeting the TGF-β signaling pathway in both neuronal and microglia cells could provide a promising therapeutic strategy in AD.

Background: Alpha-synuclein (ASyn), a marker of Parkinson's disease (PD) and other neurodegenerative processes, plays pivotal roles in neuronal nuclei and synapses. ASyn and its phosphorylated form at Serine 129 (p-ASyn) are involved in DNA protection and repair, processes altered in aging, neurodegeneration, and cancer. Objective: To analyze the localization of p-ASyn in skin biopsies of PD patients and melanoma. Methods: Biopsies from 26 PD patients, 20 melanoma patients, and 31 control subjects were probed and analyzed with a p-ASyn antibody by immunohistochemistry and immunofluorescence. Nuclear positivity was quantified by image analysis. Results: Peripheral nerve endings from healthy subjects show little p-ASyn immunopositivity but notable axonal presence in PD. Control subjects show immunopositivity to p-ASyn along all epidermic strata and scarce presence in their cytoplasm. In contrast, its nuclear presence in PD is weaker, with a higher cytoplasmic and intercellular presence. Nuclear p-ASyn in melanoma varied from similar to control skin in early stage melanoma to a higher rate of empty nuclei in the intermediate stage and total absence of nuclear p-ASyn in severe cases. Interpretation: These findings support the nuclear localization of p-ASyn in skin cells and show that its presence decreases PD and almost disappears in the malignant transformation of melanocytes, redistributing to the cytoplasm and intercellular spaces. This confirms the association between PD and melanoma, providing crucial insights into the role of p-ASyn in both diseases. Trial Registration: ClinicalTrials.gov identifier: NCT01380899.

Background: Extracellular adenosine 5'-triphosphate (ATP) acts as a signaling molecule in the peripheral nerves, regulating myelination after nerve injury. The present study examined whether the cerebrospinal fluid (CSF) ATP levels in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are related to disease severity.

Methods: CSF ATP levels in 13 patients with GBS and 18 patients with CIDP were compared with those in a control group of 16 patients with other neurological diseases (ONDs). In patients with CIDP, CSF ATP levels were compared before and after treatment. The correlations between CSF ATP levels and other factors, including clinical data and CSF protein levels, were also evaluated.

Results: Median CSF ATP levels were significantly higher in patients with GBS and CIDP than in those with ONDs. When patients with CIDP were classified into two groups depending on their responsiveness to immunotherapy, median CSF ATP levels were significantly higher in good responders than in ONDs. CSF ATP levels tended to decrease after treatment in patients with CIDP. In patients with CIDP, there is a negative correlation between CSF ATP and CSF protein levels.

Conclusions: CSF ATP levels were increased in patients with GBS and CIDP. In particular, CSF ATP levels tended to decrease following treatment in patients with CIDP. CSF ATP levels may be useful biomarkers for the diagnosis or monitoring of therapeutic effects in patients with GBS and CIDP.

Sleep disorders and fatigue represent prominent symptoms frequently experienced by individuals with multiple sclerosis (MS). Some psychological factors such as depression, stress, and anxiety seem to have a relationship with such problems. This study aimed to examine the role of depression, stress, and anxiety in predicting sleep disorders and fatigue among patients with MS. Employing a cross-sectional descriptive-correlational design, the study involved a sample size of 252 participants selected through purposive sampling based on inclusion and exclusion criteria. We utilized a demographic information questionnaire along with the Mini-Sleep Questionnaire (MSQ), Fatigue Severity Scale (FSS), and Depression, Anxiety, and Stress Scale (DASS-21) to collect data and analyzed them applying SPSS₂₂, incorporating statistical measures including Pearson correlation and regression. The results of the Pearson correlation coefficient showed that sleep disorders had a positive and significant relationship with depression (r = 0.56; P < 0.001), stress (r = 0.40; P < 0.001), and anxiety (r = 0.52; P < 0.001). There was no significant relationship between age and the development of sleep disorders in total score (r = -0.001; P < 0.985), but age had a relationship with insomnia (r = -0.146; P < 0.021) and oversleeping (r = 0.153; P < 0.015). Age and fatigue did not have a significant relationship as well (r = -0.044; P < 0.941). In addition, fatigue had a positive and significant relationship with depression (r = 0.52; P < 0.001), stress (r = 0.48; P < 0.001), and anxiety (r = 0.54; P < 0.001). The results of the regression analysis also showed that depression, stress, and anxiety predict 0.37% of the total variance of sleep disorders (F = 48.34; P < 0.001) and 0.35% of the total variance of fatigue (F = 44.64; P < 0.001). Our findings suggest that depression, stress, and anxiety play a significant role in predicting sleep disorders and fatigue among patients with MS. This study has been reported in accordance with the TREND checklist for nonrandomized trials.