International Journal of Neuroscience最新文献

Aim: Depression is characterized by pervasive cognitive and emotional disturbances, yet the neural mechanisms underlying these deficits remain incompletely understood. Method: This study utilized multimodal neuroimaging, including resting-state functional MRI and structural T1-weighted imaging, alongside the MATRICS Consensus Cognitive Battery (MCCB) and the Hamilton Depression Rating Scale (HAMD), to delineate the structural and functional alterations in the insula in first-episode, medication-naïve patients with depression. Result: Compared to matched healthy controls, patients with depression exhibited significant reductions in gray matter density in the left insula, which were robustly associated with impairments in reasoning and problem-solving abilities. Mediation analyses revealed that insular gray matter density mediated the relationship between depressive symptom severity and cognitive deficits, emphasizing the insula's critical role in linking emotional and cognitive dysfunctions. Furthermore, functional connectivity analyses identified disrupted insula-medial prefrontal cortex circuits, highlighting their contribution to the pathophysiology of depression. Conclusion: These findings underscore the insula's dual role as a structural and functional hub in depression, advancing our understanding of the neural substrates of cognitive dysfunction and informing potential targets for intervention.

Background: Previous studies have shown that an increased number of immune cells is closely associated with the onset and course changes of intracerebral hemorrhage, but the exact causal relationship has not been clarified. The aim of this study was to investigate the causal relationship between immune cells and intracerebral hemorrhage by a two-way Mendelian randomization method.

Methods: Two sets of SNPs were used as instrumental variables and two-way Mendelian randomization analyses were performed and leave-one-out method were used to assess the validity and heterogeneity of the included genetic variation instruments. The level of multiplicity and heterogeneity of the included genetic variance instruments was assessed.

Results: The results showed a clear causal relationship between three immune cells and intracerebral hemorrhage, and no heterogeneity between SNPs related to intracerebral hemorrhage, while scatterplot and funnel plot confirmed that the causality was less likely to be biased; MR-Egger results suggested that no genetic pleiotropy was found. Leave-one-out analysis was applied to suggest that the MR analysis results for a single SNP were robust; meanwhile, Meta-analysis was applied to combine the two intracerebral hemorrhage datasets, and the analysis results suggested that in the fixed-effects model and random-effects model, the immunocyte CD66b on Granulocytic Myeloid-Derived Suppressor Cells and other three immune cells were significantly causally associated with intracerebral hemorrhage, while the heterogeneity test suggested that there was no significant difference between the different datasets.

Conclusions: The present study found a significant causal relationship between specific immune cell phenotypes and intracerebral hemorrhage by Mendelian randomization analysis.

Objective: To explore the restorative effects and mechanisms of neural stem cell (NSC) transplantation on ischemic brain injury based on the Wnt signaling pathway.

Methods: Out of 102 male KM mice, 15 were randomly selected as the control group without any intervention, while the remaining 87 underwent middle cerebral artery occlusion (MCAO) using the Zea-Longa suture method. Seven mice that did not successfully model MCAO were excluded, leaving 80 mice that successfully underwent MCAO, randomized into two groups: the Ischemic Brain Injury group (n = 40) receiving 10 μL of sterile PBS solution injected into the lateral ventricle, and the Ischemic Brain Injury + NSCs Transplantation group (n = 40) receiving 10 μL of NSCs suspension injected into the lateral ventricle.

Results: Compared to the ischemic brain injury group, mice in the Ischemic Brain Injury + NSCs Transplantation group exhibited significantly alleviated edema in the middle cerebral artery supply area, with neurons displaying more normal morphological characteristics and fewer signs of degeneration and necrosis. The mice with NSC transplantation had significantly smaller infarct volume than those in the ischemic brain injury group (p < 0.05). The mice with NSC transplantation showed significantly lower Zea-Longa scores and a lower proportion of TUNEL-positive cells compared to those in the ischemic brain injury group (p < 0.05).

Conclusion: NSC transplantation can significantly inhibit neuronal apoptosis in the ischemic region of mice with ischemic brain injury, alleviate brain tissue edema, reduce infarct volume, and improve neurological function. The mechanism may be related to Wnt signaling pathway activation.

Background: The cornu ammonis 1 (CA1) region of the hippocampus is a sensitive area that is susceptible to injury caused by cerebral ischemia. High-mobility group box 1 (HMGB1) and phosphorylated c-Jun N-terminal kinase (p-JNK) play important roles in mediating cerebral ischemic injury.

Objective: To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons.

Methods: A rat model of permanent middle cerebral artery occlusion (pMCAO) was established. Sprague-Dawley rats were divided into four groups: sham-operated control, pMCAO control, EA, and sham-EA (SEA). In the EA and SEA groups, the GV20 and ST36 acupoints were selected for treatment. However, the SEA group was treated only by superficial pricking of the skin at the two acupoints without the application of electricity. Neurological function was assessed using the neurological deficit function score, and neuronal damage was detected through Nissl staining. HMGB1 and p-JNK expression was evaluated using immunohistochemical staining and western blot assays.

Results: The behavioural experiments showed that the EA treatment improved the neurological deficits in the pMCAO rats. The Nissl staining results revealed that EA reduced neural tissue damage. The immunohistochemical staining and western blot results showed that EA inhibited HMGB1 and p-JNK overexpression. By contrast, none of these EA effects were observed in the SEA group.

Conclusion: EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.

Purpose/aim of the study: This study aims to present a case of Moyamoya disease (MMD) in an adolescent who experienced a subarachnoid hemorrhage (SAH). The purpose is to underscore the importance of considering MMD as a potential cause of SAH in adolescents, particularly in the absence of common causes such as trauma or aneurysmal rupture. The case further highlights the significance of early identification and appropriate management to prevent further complications and improve patient outcomes.

Materials and methods: The diagnosis was initially based on findings from a CT angiography and later confirmed through magnetic resonance angiography (MRA) and magnetic resonance imaging (MRI).

Results: The case study demonstrates the effectiveness of utilizing MRA and MRI in diagnosing MMD in adolescents. It emphasizes the challenges in areas with limited resources where advanced imaging techniques like digital subtraction angiography (DSA) may not be readily accessible or affordable. The gold standard for MMD diagnosis, DSA, is acknowledged, but the study underscores the importance of alternative imaging methods in resource-constrained settings.

Conclusion: In conclusion, this case underscores the importance of considering Moyamoya disease as a potential etiology for subarachnoid hemorrhage in adolescents, particularly when common causes are absent. The study highlights the crucial role of MRA and MRI in the diagnosis of MMD, emphasizing their significance in areas with limited resources. Early identification and appropriate management are essential for preventing complications and improving patient outcomes, acknowledging the challenges associated with the accessibility of gold standard diagnostic techniques in certain settings.

Purpose/aim: The developing brain undergoes a remarkable process of synaptic changes.

Material and methods: To investigate the developmental changes in glutamatergic synaptic connections using the whole-cell patch clamp method, evoked excitatory postsynaptic currents (eEPSCs) were recorded from locus coeruleus (LC) neurons, a brain region crucial for cognitive functions, in rats at ages 7, 14, and 21 days. We employed fractal analysis to compute fractal dimensions of AMPA and NMDA receptors, serving as markers for synaptic maturation.

Results: Our findings revealed a significant increase in fractal dimensions during the third postnatal week and hence a developmental chenge of synaptic connections. A strong positive correlation between amplitude and fractal dimensions, in Pearson correlation analysis suggested that the synaptic currents' amplitude is closely related to the fractal properties of the receptors. A linear relationship between fractal dimensions and age indicated that fractal analysis can be a robust tool for predicting developmental changes. Additionally, we employed machine learning techniques to predict developmental changes based on AMPA and NMDA receptors. Support Vector Machine (SVM) models outperformed random forest models in accurately predicting age-dependent developmental changes, as indicated by the area under the curve (AUC) values. SVM achieved an AUC of 0.89 for AMPA receptors and 0.86 for NMDA receptors, demonstrating the effectiveness of fractal-based features in characterizing synaptic maturation.

Conclusion: This study offers valuable insights into synaptic development in the LC nucleus and demonstrates the potential of fractal analysis as a tool to understand brain plasticity and early development. Fractal dimensions play a crucial role in characterizing the maturation of glutamatergic synapses and neural circuitry development.

Purpose: To investigate the activity of default mode network (DMN), frontoparietal network (FPN) and cerebellar network (CN) in drug-resistant epilepsy (DRE) patients undergoing vagus nerve stimulation (VNS).

Methods: Fifteen patients were recruited and underwent resting-state functional magnetic resonance imaging (fMRI) scans. Independent component analysis and paired sample t-tests were used to examine activity changes of DMN, FPN and CN before and after VNS.

Results: Compared with preoperative patients, DMN exhibited decreased activity in left cuneus/precuneus, left median cingulate gyrus, left superior/middle occipital gyrus, right superior parietal gyrus, right precentral/postcentral gyrus, right rolandic operculum and right insula, while increased activity was observed in right supramarginal gyrus, left fusiform gyrus, right supplementary motor area, left amygdala, and right inferior frontal gyrus. FPN displayed decreased activity in left cuneus, left anterior cingulate gyrus, right precentral gyrus, left middle/inferior frontal gyrus, right middle frontal gyrus, left superior/middle temporal gyrus, left superior/middle occipital gyrus, and right superior parietal gyrus, but increased activity in right inferior temporal gyrus. CN showed decreased activity in left superior/middle frontal gyrus, right inferior frontal gyrus, left supplementary motor area, left precuneus, left postcentral gyrus, left middle occipital gyrus, right middle temporal gyrus, and left inferior cerebellum, while increased activity was detected in bilateral superior cerebellum and right fusiform gyrus.

Conclusions: DMN, FPN and CN exhibited distinct changes in DRE patients following VNS. The suppression or activation of sensorimotor, language, memory and emotion-related regions may represent the underlying neurological mechanisms of VNS. However, the contrasting activity patterns between superior and inferior cerebellum require further investigation.

Nerve injury can be caused by a variety of factors. It often takes a long time to repair a nerve injury and severe nerve injury is even difficult to heal. Therefore, increasing attention has focused on nerve injury and repair. Long non-coding RNA (lncRNA) is a newly discovered non-coding RNA with a wide range of biological activities. Numerous studies have shown that a variety of lncRNAs undergo changes in expression after nerve injury, indicating that lncRNAs may be involved in various biological processes of nerve repair and regeneration. Herein, we summarize the biological roles of lncRNAs in neurons, glial cells and other cells during nerve injury and regeneration, which will help lncRNAs to be better applied in nerve injury and regeneration in the future.

Background: Stunting become a global concern because it's not only affecting physical stature, but also affecting on neurodevelopment and cognitive function. These impacts are resulting in long-term consequences especially for human resources, such as poor-quality labor, decreased productivity due to decreasing of health quality, including immunity and cognitive aspect.

Discussion: This comprehensive review found that based on many studies, there is an altered gut microbiota, or dysbiosis, in stunted children, causing the impairment of brain development through Microbiota-Gut Brain Axis (MGB Axis) mechanism. The administration of probiotics has been known affect MGBA by improving the physical and chemical gut barrier integrity, producing antimicrobial substance to inhibit pathogen, and recovering the healthy gut microbiota. Probiotics, along with healthy gut microbiota, produce SCFAs which have various positive impact on CNS, such as increase neurogenesis, support the development and function of microglia, reduce inflammatory signaling, improve the Blood Brain Barrier's (BBB's) integrity, produce neurotropic factors (e.g. BDNF, GDNF), and promote the formation of new synapse. Probiotics also could induce the production of IGF-1 by intestinal epithelial cells, which functioned as growth factor of multiple body tissues and resulted in improvement of linear growth as well as brain development.

Conclusion: These properties of probiotics made it become the promising and feasible new treatment approach for stunting. But since most of the studies in this field are conducted in animal models, it is necessary to translate animal data into human models and do additional study to identify the numerous components in the MGB axis and the effect of probiotics on human.

Objective: To identify the molecular targets of mesenchymal stem cell (MSC)-derived exosomes in treating cerebral ischemia and elucidate their therapeutic mechanisms.

Methods: We utilized a mouse model of middle cerebral artery occlusion and treated mice with umbilical cord mesenchymal stem cells derived exosomes. Proteomic analysis identified AAK1(AP2 associated kinase 1) as a key target protein. Functional studies confirmed that AAK1 modulates the NF-κB signaling pathway in ischemic stroke. MicroRNA profiling, bioinformatic prediction and cell experiments identified miR-664a-5p as the specific microRNA regulating AAK1 expression. Finally, we validated the therapeutic effects of umbilical cord mesenchymal stem cell-derived exosomes using engineered miR-664a-5p-deficient exosomes.

Results: Our findings demonstrate that umbilical cord mesenchymal stem cells-derived exosomes exert neuroprotective effects in ischemic stroke by modulating the AAK1/NF-κB axis via miR-664a-5p.

Conclusion: This study provides novel insights into the therapeutic mechanism of mesenchymal stem cell-derived exosomes in ischemic stroke, highlighting their potential for developing exosome-based therapies.