Journal of Neurorestoratology最新文献

Objective

Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.

Methods

We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.

Results

GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.

Conclusion

GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.

Depression is a mental disease that involves a variety of complex physiological mechanisms. A wide range of methods have therefore been used to establish mouse models of depression, and there are currently many ways to develop such mouse models. The present study aimed to compare the effects of various model induction methods and assesses their different effects. To this end, C57BL/6J mice were divided into three experimental groups: the chronic restraint stress (CRS) group received 6 hours of daily confinement within restraint tubes over a 3-week period; the chronic lipopolysaccharide (C-LPS) administration group received daily intraperitoneal injections of 0.5 mg/kg LPS for 1 week; and the acute LPS (A-LPS) administration group received a singular intraperitoneal injection of 0.83 mg/kg LPS. A corresponding control group was established for each experimental condition. Following mouse model establishment, depression-like behaviors were assessed through the forced swimming and tail suspension tests; anxiety-related behaviors were evaluated using the open field test and elevated plus maze. Furthermore, the expression of the immediate early gene c-Fos, ionized calcium-binding adapter molecule 1 (IBA1), and glial fibrillary acidic protein (GFAP) was examined via immunofluorescence. Longer immobility durations during the forced swimming and tail suspension tests were observed across all model groups (p < 0.05), indicating depression-like behaviors. Furthermore, the CRS and C-LPS group, but not the A-LPS group, showed significant anxiety-like behaviors in the elevated plus maze (p < 0.05). All model groups also exhibited significant increases in both time and distance explored within the central area of the open field test (p < 0.05). The activation of GFAP- and IBA1-positive cells in the cerebral cortex and hippocampus was also markedly pronounced in all experimental groups, suggesting the association of neuroinflammatory responses with induced depressive states. The present findings contribute to our understanding of the pathophysiology of stress-induced and neuroinflammatory-associated depression, and will help researchers to choose suitable depression models for their investigations.

Remarkable advancements have been made in understanding the pathogenesis of Alzheimer's disease, Parkinson's disease, and other neurological disease; in our depth of understanding neurorestorative mechanisms such as anti-inflammatory processes, immune regulation, neuromodulation, neovascularization/neural repair, and neuroprotection; and in clinical neurorestorative treatments. Multiple types of cell therapies have been reported, with some positive outcomes. Diverse forms of neurostimulation and neuromodulation as well as brain–computer interfaces have shown good therapeutic outcomes in clinical applications. Further, therapeutic neurorestorative surgery and pharmaceutic therapy have been very impressive. These fundamental achievements are helpful for understanding the pathogenesis of neurological diseases and the mechanisms of neurorestoration. Patients with neurological impairments have benefited from therapeutic progress, but some of these therapies still require confirmation in higher-level randomized clinical trials.

Background

Ultrashort wave (USW) therapy has been reported to alleviate cerebral ischemia/reperfusion (IR) injury, however the underlying mechanisms remain elusive. The aim of this study was to observe the effect of non-thermal USW therapy on neuronal damage and expression of heat shock protein 70 (HSP70) after cerebral IR in rats.

Methods

Focal ischemia-reperfusion (IR) was induced in Sprague–Dawley rats by middle cerebral artery occlusion/reperfusion (MCAO/R). The Ninety-two rats (both male and female) were screened using the Zea-Longa 5 grade evaluation. Included rats were then randomly divided into blank, sham, model 1-day, model 3-day, model 7-day, USW 1-day, USW 3-day, or USW 7-day groups. All rats in the model groups received sham USW treatment, while rats in the USW groups received USW treatment, for 1, 3, or 7 days. We assessed the National Institutes of Health Stroke Scale, brain infarction volumes, ultrastructural damage scores using electron microscopy, and HSP70 expression by western blotting between the different groups.

Results

USW treatment reduced the National Institutes of Health Stroke Scale, infarction volume, and ultrastructural neuronal damage, and increased expression of HSP70, in the hippocampal CA1 region.

Conclusions

Non-thermal USW therapy may improve neurological function, decrease infarction volume, and reduce neuronal damage by increasing HSP70 expression following cerebral IR injury.

Stroke survivors often experience debilitating neural, physical, and cognitive impairments, particularly affecting upper limb functions. Conventional rehabilitations, though effective, are perceived as slow and monotonous by stroke survivors. This review explores the potential of Virtual Reality (VR) as an engaging rehabilitation approach to address such limitations. Our findings show that VR-based rehabilitations can be beneficial in restoring post-stroke upper limb functions and improving routine life of survivors. Moreover, VR offers adaptability, and user-friendliness across age groups. However, further research with larger sample size studies and stronger evidence base is needed to definitively establish the effectiveness of VR in post-stroke rehabilitation.

Restoring function to peripheral nerves with a gap is challenging, with <50% of patients undergoing nerve repair surgery recovering function. Sensory nerve grafts (autografts) are the clinical “gold standard” for bridging nerve gaps to restore sensory and motor function. They have significant limitations and restore meaningful function only across short gaps when repairs are performed soon after trauma and patients are young. When the value of any of these variables is large, the extent of recovery decreases precipitously, and when two or all are simultaneously large, there is little to no recovery. The extent of restored meaningful recovery has not increased in almost 70 years. Thus, novel techniques are needed that enhance both the extent of recovery and the percentage of patients who recover meaningful recovery. This paper reviews the limitations of autografts and other materials used to repair nerves. It also examines autologous platelet-rich plasma (PRP), a promising nerve gap repair technique that induces recovery in clinical settings where autografts are ineffective, including when the values of all three variables are simultaneously large.