Neurology Research International最新文献

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.

Finding reliable biomarkers has a crucial role in Parkinson's disease (PD) assessments. Saliva is a bodily fluid, which might be used as a source of biomarkers for PD. Our article has reviewed several publications on salivary proteins in PD patients and their potential as biomarkers. We find out that α-Syn's proportion in oligomeric form is higher in PD patients' saliva, which is potent to use as a biomarker for PD. The salivary concentration of DJ-1 and alpha-amylase is lower in PD patients. Also, substance P level is more moderate in PD patients. Although salivary flow rate is decreased in PD patients, high levels of heme oxygenase and acetylcholinesterase might be used as noninvasive biomarkers. Salivary miRNAs (miR-153, miR-223, miR-874, and miR-145-3p) are novel diagnostic biomarkers that should be given more attention.

40-70% of patients after a stroke, including a mild one, may experience cognitive impairment. Brain-derived neurotrophic factor (BDNF) plays a significant role in the pathogenesis and rehabilitation of ischemic stroke and also affects the patients' recovery prognosis. An association between cognitive impairment in the poststroke period and lower peripheral BDNF levels is known, but the prognostic significance of serum BDNF levels and clinical characteristics for the risk of developing cognitive impairment in the acute period remains uncertain. We conducted a prospective cohort study of patients in the acute phase of ischemic stroke. Clinical examination, assessment of neurological status, neuropsychological testing, and laboratory analyzes were performed on patients at 1 and 14 days after ischemic stroke. The state of cognitive functions was assessed by the Mini-Mental State Examination scale. Quantification of BDNF in blood serum was performed by solid-phaseenzyme-linked immunosorbent assay (ELISA). We found that within 14 days after an acute ischemic stroke, we found a decrease in the clinical severity of patients compared to 1 day of the onset of the disease before the start of treatment and a significant decrease in the level of BDNF in the blood serum of patients with ischemic stroke both on the first and on the 14th day. However, during the 2 weeks of the acute period, no significant changes were detected, despite the general improvement of the clinical condition. In our study, cognitive impairment was found in almost half of the patients on the first day of ischemic stroke, and there was no significant reduction in this prevalence over 2 weeks. We found that a low level of BDNF and a thrombotic subtype of ischemic stroke can be risk factors for cognitive impairment in the acute period, which can be useful in planning treatment and rehabilitation measures.