Journal of Neurorestoratology最新文献

Background

Depression, also known as major depressive disorder, is a mental disorder caused by multiple factors. The cause of depression remains unclear, but a growing number of studies have reported a link between depression and long non-coding RNAs (lncRNAs). In the present study, we reviewed the relationships between depression and four lncRNAs, focusing on the differential expression of these lncRNAs in patients with depression, how to regulate depression, and how to use lncRNAs for the diagnosis, prevention, and treatment of clinical depression.

Methods

A systematic review of 23 studies published between 2011 and 2021 was conducted using Pubmed. Selection criteria included publication date and relevance to topic: Only articles published after 2010 were included to ensure the review reflects the most recent research, and all articles are selected strictly on their research topic.

Results

The short communication has summarized the relationships between depression and four lncRNAs, especially antisense lncRNAs and lincRNAs, and their potential in the diagnosis of depression and its targeted therapy.

Conclusions

The study found that these four lncRNAs, particularly antisense lncRNAs and lincRNAs, are closely associated with various aspects of depression. These findings suggest new therapeutic targets and could contribute to improving the accuracy of depression diagnosis.

Traumatic brain injury (TBI) and lifestyle habits such as Western diet (WD) consumption represent two risk factors that affect an individual's health outcome globally. Individuals with TBI have a greater risk of mortality from associated chronic diseases than the general population. WD has been shown to impair cognitive function, decrease the brain's capacity to compensate for insult by affecting recovery as well as induce metabolic syndrome (MetS) which may be a risk factor for poor TBI prognosis. Hence, this study aims to investigate the impact of WD on TBI behavioral outcomes and neuropathology. Eight-week-old male C57BL6 mice were fed either WD or normal chow for 4 weeks prior to TBI induction. At week four, mice underwent either an experimental open-head TBI or a sham procedure. Mice continued their respective diets for four weeks after brain injury. Metabolic, cognitive function, and molecular assessment were performed four weeks after TBI. Results showed that while WD significantly increased fat percentage and elevated plasma cholesterol, there was no change in blood glucose level or body weight, indicating an early stage of MetS. Nevertheless, this was associated with neuroinflammation and impaired cognitive functions. However, there was no significant impact on cardiovascular function and mitochondrial bioenergetics. Importantly, the mild MetS induced by WD triggered basal motor, cognitive deterioration and exacerbated the long-term neuropathology of TBI. Taken together, our work highlights the magnitude of the contribution of lifestyle factors including the type of diet, even in the absence of overt metabolic consequences, on the neurobehavioral prognosis following TBI.

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.

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.

Objective

To evaluate the efficacy and safety of combining troxerutin and cerebroprotein hydrolysate (TCH) for treating acute cerebral infarction via a systematic review.

Methods

The computer-based search encompassed eight databases—PubMed, Cochrane Library, Embase, Web of Science, China Biomedical Literature Database, China National Knowledge Infrastructure, Wanfang Data, and China Science and Technology Journal Database—from their establishment until December 2023. Randomized controlled trials that assessed TCH for acute cerebral infarction were selected according to inclusion and exclusion criteria. The data extraction, data quality evaluation, and meta-analysis were performed using RevMan 5.4.1 software.

Results

The analysis incorporated 18 studies encompassing 1,957 cases. Compared with the control group, the TCH treatment group had superior outcomes in effective rates (risk ratio [RR] = 1.24, 95% confidence interval [CI; 1.18, 1.30], Z = 8.84, p < 0.05), neurological deficit scores (mean difference [MD] = −3.71, 95% CI [−4.32, −3.10], Z = 11.92, p < 0.05), activity of daily living scores (MD = 13.32, 95% CI [11.66, 14.98], Z = 15.75, p < 0.05), changes in low shear viscosity (MD = −1.82, 95% CI [−2.57, −1.06], Z = 4.73, p < 0.05), and plasma fibrinogen levels (MD = −0.43, 95% CI [−0.47, −0.39], Z = 20.01, p < 0.05). However, there was no significant difference in adverse reaction between the two groups (RR = 0.72, 95% CI [0.45, 1.14], Z = 1.39, p = 0.16). No severe adverse drug reactions were observed in either group.

Conclusion

Combined TCH is effective and safe for treating acute cerebral infarction.

Background

C-type natriuretic peptide (CNP) can be altered during stress and has protective effects in both the heart and brain; the functions of both organs can be positively affected by CNP modulation. Low arousal sounds can modulate heart–brain communication and improve stress responses. Here, we aimed to explore the modulation of CNP and glial fibrillary acidic protein (GFAP) and neuroprotective effects of low arousal theta frequency sound (TFS).

Methods

Chronic stress was induced in mice (n > 4) using four different stressors on alternate days for 15 days, followed by TFS therapy on alternate days. Open field and elevated plus maze tests were administered for the behavioral analysis, and enzyme-linked immunosorbent assay was used to analyze corticosterone, dopamine, and serotonin levels. Hematoxylin and eosin and cresyl violet staining were used for the morphological analysis of brain and heart sections, and immunohistochemistry for GFAP and CNP was performed.

Results

TFS significantly increased the time spent in the open arms during the elevated plus maze (p < 0.05) and improved exploration in the open field test (p < 0.05). In both tests, decision-making times were significantly reduced by TFS. Nuclear morphology and GFAP expression demonstrated significantly reduced gliosis in fear pathways after TFS therapy x. CNP levels were restored in fear pathways but not intrinsic cardiac ganglia (responsible for heart–brain communication) in TFS-treated mice. Brain corticosterone and dopamine levels increased after TFS therapy, reflecting restored motivational behaviors.

Conclusions

Low arousal TFS is a potential neuromodulator for treating stress and related complications.

STXBP1 encephalopathy (STXBP1-E) is a rare neurodevelopmental disorder that includes epilepsy; it is caused by de novo STXBP1 mutations. In clinical settings, pharmaceutical interventions to treat STXBP1-E predominantly concentrate on seizure control. However, effective treatments for seizure recurrence, treatment resistance, and common comorbidities remain scarce. Patients with STXBP1-E display a wide range of pathogenic variations that manifest as loss-of-function, gain-of-function, or dominant-negative effects. However, recent studies have primarily investigated the pathogenic mechanisms resulting from loss-of-function mutations using STXBP1 haploinsufficiency models. This approach fails to accurately assess the impact of disease-causing mutations. Moreover, to evaluate new syntaxin-binding protein 1 (STXBP1)-targeting drugs, novel models that incorporate disease-causing mutations or even the genetic backgrounds of patients are needed. Here, we discuss the clinical symptoms of STXBP1-E and the relationship between this disorder and STXBP1 mutations. We also review recent progress toward understanding the biological function of STXBP1 and its deficiency-induced cellular defects. We then discuss recent discoveries concerning the pathogenesis of STXBP1-E and the limitations and challenges associated with the current research model. Additionally, we underscore the value of leveraging stem cell technology to study the pathogenic mechanisms of STXBP1-E, and review stem cell transplantation as a potential approach for treating this disorder. We also discuss potential future research directions that need to be resolved.

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.