Neural Plasticity最新文献

The blood-brain barrier (BBB) is a semipermeable and extremely selective system in the central nervous system of most vertebrates, that separates blood from the brain's extracellular fluid. It plays a vital role in regulating the transport of necessary materials for brain function, furthermore, protecting it from foreign substances in the blood that could damage it. In this review, we searched in Google Scholar, Pubmed, Web of Science, and Saudi Digital Library for the various cells and components that support the development and function of this barrier, as well as the different pathways to transport the various molecules between blood and the brain. We also discussed the aspects that lead to BBB dysfunction and its neuropathological consequences, with the identification of some of the most important biomarkers that might be used as a biomarker to predict the BBB disturbances. This comprehensive overview of BBB will pave the way for future studies to focus on developing more specific targeting systems in material delivery as a future approach that assists in combinatorial therapy or nanotherapy to destroy or modify this barrier in pathological conditions such as brain tumors and brain stem cell carcinomas.

This study is aimed at investigating the potential roles of G protein-coupled estrogen receptor 1 (GPER, also known as GPR30) in the preventive effect of ginsenoside Rg1 against cognitive impairment and hippocampal cell apoptosis in experimental vascular dementia (VD) in mice. The effects of bilateral common carotid artery stenosis (BCAS) on GPR30 expression at mRNA level were evaluated. Thereafter, the BCAS mouse model was utilized to evaluate the protection of Rg1 (0.1, 1, 10 mg/kg, 14 days, ip). Spatial memory was evaluated by water Morris Maze 7 days post BCAS. After behavioral tests, neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and potential mechanisms were determined using western blotting and quantitative real-time PCR. Our results showed that GPR30 expression in the hippocampal region at mRNA level was promoted 30 min, 3 h, 6 h, and 24 h following BCAS. Ginsenoside Rg1 (1 or 10 mg/kg, 14 days, ip) promoted GPR30 expression in the hippocampus of model mice (after behavioral tests) but did not alter GPR30 expression in the hippocampus of control mice. Moreover, treatment of ginsenoside Rg1 (10 mg/kg) or G1 (5 μg/kg), a GPR30 agonist, prevented BCAS-induced memory impairment and hippocampal neuronal loss and apoptosis and promoted the ratio of Bcl-2 to Bax expression in the hippocampus (after behavioral tests). On the contrary, G15 (185 μg/kg), an antagonist of GPR30, aggravated BCAS-induced hippocampal neuronal loss and apoptosis. Finally, drug-target molecular docking pointed that Rg1 had a lower binding energy with GPR30 compared with Bax and Bcl-2. Together, our data implicate that ginsenoside Rg1 prevents cognitive impairment and hippocampal neuronal apoptosis in VD mice, likely through promoting GPR30 expression. These results would provide important implications for the application of Rg1 in the treatment of VD.

Circular RNAs (circRNAs) are highly enriched in the central nervous system and significantly involved in a range of brain-related physiological and pathological processes. Ischemic stroke is a complex disorder caused by multiple factors; however, whether brain-derived circRNAs participate in the complex regulatory networks involved in stroke pathogenesis remains unknown. Here, we successfully constructed a cerebral ischemia-injury model of middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats. Preliminary qualitative and quantitative analyses of poststroke cortical circRNAs were performed through deep sequencing, and RT-PCR and qRT-PCR were used for validation. Of the 24,858 circRNAs expressed in the rat cerebral cortex, 294 circRNAs were differentially expressed in the ipsilateral cerebral cortex between the MCAO and sham rat groups. Cluster, GO, and KEGG analyses showed enrichments of these circRNAs and their host genes in numerous biological processes and pathways closely related to stroke. We selected 106 of the 294 circRNAs and constructed a circRNA-miRNA-mRNA interaction network comprising 577 sponge miRNAs and 696 target mRNAs. In total, 15 key potential circRNAs were predicted to be involved in the posttranscriptional regulation of a series of downstream target genes, which are widely implicated in poststroke processes, such as oxidative stress, apoptosis, inflammatory response, and nerve regeneration, through the competing endogenous RNA mechanism. Thus, circRNAs appear to be involved in multilevel actions that regulate the vast network of multiple mechanisms and events that occur after a stroke. These results provide novel insights into the complex pathophysiological mechanisms of stroke.

Background: Postinterventional cerebral hyperdensity (PCHD) is commonly seen in acute ischemic patients after mechanical thrombectomy. We propose a new classification of PCHD to investigate its correlation with hemorrhagic transformation (HT). The clinical prognosis of PCHD was further studied.

Methods: Data from 189 acute stroke patients were analyzed retrospectively. According to the European Cooperative Acute Stroke Study criteria (ECASS), HT was classified as hemorrhagic infarction (HI-1 and HI-2) and parenchymal hematoma (pH-1 and pH-2). Referring to the classification of HT, PCHD was classified as PCHD-1, PCHD-2, PCHD-3, and PCHD-4. The prognosis included early neurological deterioration (END) and the modified Rankin Scale (mRS) score at 3 months.

Results: The incidence of HT was 14.8% (12/81) in the no-PCHD group and 77.8% (84/108) in the PCHD group. PCHD was highly correlated with HT (r = 0.751, p < 0.01). After stepwise regression analysis, PCHD and the National Institutes of Health Stroke Scale (NIHSS) score at admission were found to be independent factors for END (p < 0.001, p = 0.015, respectively). The area of curves (AUC) of PCHD, the NIHSS at admission, and the combined model were 0.810, 0.667, and 0.832, respectively. The optimal diagnostic cutoff of PCHD for END was PCHD > 2. PCHD, the NIHSS score at admission, and good vascular recanalization (VR) were independently associated with 3-month mRS (all p < 0.05). The AUC of PCHD, the NIHSS at admission, good VR, and the combined model were 0.779, 0.733, 0.565, and 0.867, respectively. And the best cutoff of PCHD for the mRS was PCHD > 1.

Conclusion: The relationship of PCHD and HT suggested PCHD was an early risk indicator for HT. The occurrence of PCHD-3 and PCHD-4 was a strong predictor for END. PCHD-1 is considered to be relatively benign in relation to the 3-month mRS.

Objective: To study the changes in gait characteristics of stroke patients with foot drop after the combination treatment of foot drop stimulator and moving treadmill training and thus provide a basis for the improvement in a foot drop gait after stroke.

Methods: Sixty patients with hemiplegia and foot drop caused by stroke were randomly divided into two groups of 30: the test group and the control group. Both groups received basic rehabilitation training. On this basis, the test group received the combination treatment of foot drop stimulator and moving treadmill training. The control group received foot drop stimulator training. Both groups received consecutive treatment for 3 weeks, five times a week, and every single time lasted for 30 minutes. Before and after the treatment, a gait watch three-dimensional gait analysis system was used to measure and record the maximum angles of flexion of the affected side's hip, knee, and ankle; the pace; the step length asymmetry; the iEMG of the tibialis anterior muscle; the functional ambulation category; and Ashworth's modified spasticity classification of the gastrocnemius.

Results: After treatment, in the two groups, the maximum angles of flexion of the affected side's hip, knee, and ankle improved, the pace increased, the step length asymmetry decreased, the iEMG of the tibialis anterior muscle increased, the functional ambulation category improved, and Ashworth's modified spasticity classification of the gastrocnemius decreased, but the above changes in the test group were better than those in the control group. The difference is statistically significant (p < 0.05).

Conclusions: The combination treatment of the foot drop stimulator and moving treadmill can significantly improve stroke patients' foot gait and promote the normalization of hip flexion, knee flexion, and ankle flexion. It can increase the pace, significantly reduce the step length asymmetry, reduce the muscle tone of the gastrocnemius, and improve walking function.

The objective of this study was to systematically review the literature on the effects of cognitive behavioral therapy (CBT) on insomnia and pain in patients with traumatic brain injury (TBI). PubMed, Embase, the Cochrane Library, Cumulative Index to Nursing and Allied Health, and Web of Science databases were searched. Outcomes, including pain, sleep quality, and adverse events, were investigated. Differences were expressed using mean differences (MDs) with 95% confidence intervals (CIs). The statistical analysis was performed using STATA 16.0. Twelve trials with 476 TBI patients were included. The included studies did not indicate a positive effect of CBT on pain. Significant improvements were shown for self-reported sleep quality, reported with the Pittsburgh Self-Reported Sleep Quality Index (MD, -2.30; 95% CI, -3.45 to -1.15; P < 0.001) and Insomnia Severity Index (MD, -5.12; 95% CI, -9.69 to -0.55; P = 0.028). No major adverse events related to CBT were reported. The underpowered evidence suggested that CBT is effective in the management of sleep quality and pain in TBI adults. Future studies with larger samples are recommended to determine significance. This trial is registered with PROSPERO registration number CRD42019147266.

Background: Dysphagia is a common sequelae after stroke. Noninvasive brain stimulation (NIBS) is a tool that has been used in the rehabilitation process to modify cortical excitability and improve dysphagia.

Objective: To systematically evaluate the effect of NIBS on dysphagia after stroke and compare the effects of two different NIBS.

Methods: Randomized controlled trials about the effect of NIBS on dysphagia after stroke were retrieved from databases of PubMed, Embase, Cochrane Library, Web of Science, CNKI, Wanfang Data, VIP, and CBM, from inception to June 2021. The quality of the trials was assessed, and the data were extracted according to the Cochrane Handbook for Systematic Reviews of Interventions. A statistical analysis was carried out using RevMan 5.3 and ADDIS 1.16.8. The effect size was evaluated by using the standardized mean difference (SMD) and a 95% confidence interval (CI).

Results: Ultimately, 18 studies involving 738 patients were included. Meta-analysis showed that NIBS could improve the dysphagia outcome and severity scale (DOSS) score (standard mean difference (SMD) = 1.44, 95% CI 0.80 to 2.08, P < 0.05) and the water swallow test score (SMD = 6.23, 95% CI 5.44 to 7.03, P < 0.05). NIBS could reduce the standardized swallowing assessment (SSA) score (SMD = -1.04, 95% CI -1.50 to -0.58, P < 0.05), the penetration-aspiration scale (PAS) score (SMD = -0.85, 95% CI -1.33 to -0.36, P < 0.05), and the functional dysphagia scale score (SMD = -1.05, 95% CI -1.48 to -0.62, P < 0.05). Network meta-analysis showed that the best probabilistic ranking of the effects of two different NIBS on the DOSS score is rTMS (P = 0.52) > tDCS (P = 0.48), the best probabilistic ranking of the SSA score is rTMS (P = 0.72) > tDCS (P = 0.28), and the best probabilistic ranking of the PAS score is rTMS (P = 0.68) > tDCS (P = 0.32).

Conclusion: Existing evidence showed that NIBS could improve swallowing dysfunction and reduce the occurrence of aspiration after stroke, and that rTMS is better than tDCS. Limited by the number of included studies, more large-sample, multicenter, double-blind, high-quality clinical randomized controlled trials are still needed in the future to further confirm the results of this research.

Attention bias (AB) is a common cognitive challenge for patients with pain. In this study, we tested at what stage AB to pain occurs in participants with experimental pain (EP) and tested whether cognitive load interferes with it. We recruited 40 healthy adults aged 18-27 years, and randomized them into control and EP groups. We sprayed the participants in the EP group with 10% capsaicin paste to mimic acute pain and those in the control group with water, accessing both groups' behavioral results and event-related potential data. We found that high-load tasks had longer response times and lower accuracies than low-load tasks did and that different neural processing of words occurred between the groups. The EP group exhibited AB to pain at an early stage with both attentional avoidance (N1 latency) and facilitated attention (P2 amplitude) to pain words. The control group coped with semantic differentiation (N1) at first, followed by pain word discrimination (P2). In addition, AB to pain occurred only in low-load tasks. As the cognitive load multiplied, we did not find AB in the EP group. Therefore, our study adds further evidence for AB to pain, suggesting the implementation of cognitive load in future AB therapy.

This study introduced new MRI techniques such as neurite orientation dispersion and density imaging (NODDI); NODDI applies a three-compartment tissue model to multishell DWI data that allows the examination of both the intra- and extracellular properties of white matter tissue. This, in turn, enables us to distinguish the two key aspects of axonal pathology-the packing density of axons in the white matter and the spatial organization of axons (orientation dispersion (OD)). NODDI is used to detect possible abnormalities of posttraumatic encephalomalacia fluid-attenuated inversion recovery (FLAIR) hyperintense lesions in neurite density and dispersion. Methods. 26 epilepsy patients associated with FLAIR hyperintensity around the trauma encephalomalacia region were in the epilepsy group. 18 posttraumatic patients with a FLAIR hyperintense encephalomalacia region were in the nonepilepsy group. Neurite density and dispersion affection in FLAIR hyperintense lesions around encephalomalacia were measured by NODDI using intracellular volume fraction (ICVF), and we compare these findings with conventional diffusion MRI parameters, namely, fractional anisotropy (FA) and apparent diffusion coefficient (ADC). Differences were compared between the epilepsy and nonepilepsy groups, as well as in the FLAIR hyperintense part and in the FLAIR hypointense part to try to find neurite density and dispersion differences in these parts. Results. ICVF of FLAIR hyperintense lesions in the epilepsy group was significantly higher than that in the nonepilepsy group (P < 0.001). ICVF reveals more information of FLAIR(+) and FLAIR(-) parts of encephalomalacia than OD and FA and ADC. Conclusion. The FLAIR hyperintense part around encephalomalacia in the epilepsy group showed higher ICVF, indicating that this part may have more neurite density and dispersion and may be contributing to epilepsy. NODDI indicated high neurite density with the intensity of myelin in the FLAIR hyperintense lesion. Therefore, NODDI likely shows that neurite density may be a more sensitive marker of pathology than FA.

Spinal cord stimulation (SCS) as an evidence-based interventional treatment has been used and approved for clinical use in a variety of pathological states including peripheral neuropathic pain; however, until now, it has not been used for the treatment of spinal cord injury- (SCI-) induced central neuropathic pain. This paper reviews the underlying mechanisms of SCS-induced analgesia and its clinical application in the management of peripheral and central neuropathic pain. Evidence from recent research publications indicates that nociceptive processing at peripheral and central sensory systems is thought to be modulated by SCS through (i) inhibition of the ascending nociceptive transmission by the release of analgesic neurotransmitters such as GABA and endocannabinoids at the spinal dorsal horn; (ii) facilitation of the descending inhibition by release of noradrenalin, dopamine, and serotonin acting on their receptors in the spinal cord; and (iii) activation of a variety of supraspinal brain areas related to pain perception and emotion. These insights into the mechanisms have resulted in the clinically approved use of SCS in peripheral neuropathic pain states like Complex Regional Pain Syndrome (CRPS) and Failed Back Surgery Syndrome (FBSS). However, the mechanisms underlying SCS-induced pain relief in central neuropathic pain are only partly understood, and more research is needed before this therapy can be implemented in SCI patients with central neuropathic pain.