Journal of Neuroscience Research最新文献

Regenerative medicine aims to restore damaged tissues or organs using stem cells, biomaterials, and decellularized grafts. Peripheral nerve injuries (PNI), affecting 2.8% of patients, lead to severe functional impairments with global socioeconomic costs exceeding $7 billion annually. Despite advancements in surgical techniques, full functional recovery remains elusive, particularly in critical gap injuries (> 3 cm). Autografts remain the gold standard but are hindered by donor tissue scarcity and complications like neuroma formation. Allografts face challenges due to the lack of Schwann cells and neurotrophic support. Emerging approaches in tissue engineering leverage synthetic materials, such as polycaprolactone (PCL) and polylactic acid (PLA), and biological scaffolds like decellularized nerve grafts. These innovations provide structural support, promote axonal regeneration, and retain extracellular matrix components, enabling cell adhesion and migration while minimizing antigenicity. However, barriers such as mechanical instability, scar tissue formation, and inadequate cellularization persist. This review explores the anatomy and clinical significance of the sciatic nerve, historical perspectives on peripheral nerve repair, and current treatment strategies. It evaluates biological and synthetic nerve conduits, highlighting FDA-approved products and their advantages in promoting nerve regeneration. Additionally, the paper discusses challenges in the field, including limited functional recovery and the need for more effective clinical solutions. By combining natural and synthetic materials with growth factor delivery and vascularization strategies, engineered scaffolds hold promise for improving outcomes in PNI repair. Further research is essential to optimize these technologies and bridge existing gaps in clinical practice.

Chronic epilepsy is mainly characterized by spontaneous recurrent seizures (SRS). The peroxisome proliferator activated receptor gamma/phosphatase and tensin homolog/protein kinase B (PPARγ/PTEN/Akt) pathway is involved in the pathogenesis of SRS and neuronal loss. Curcumin is a natural compound, and previous studies have shown it provides neuroprotection via anti-inflammation and anti-oxidant effects in many central nervous system (CNS) diseases. In the present study, we show that curcumin regulates the abnormal expression of PTEN and Akt in the SRS phase, improves the neuronal loss in the hippocampus, and suppresses SRS development and seizure spike activity in epileptic rats. More importantly, these effects are reversed by the PPARγ antagonist, T0070907, suggesting that curcumin exerts neuroprotective and anti-epileptic effects through the PPARγ/PTEN/Akt signaling pathway. Other studies have shown that curcumin can cross the BBB and has a safety profiles and pleiotropic pharmacological effects. Thus, our data support the proposition that curcumin might be a potential neuroprotective and anti-epileptic agent for chronic epilepsy.

Glioma is the most common primary brain tumor, characterized by high invasiveness and poor prognosis. The purinergic ligand-gated ion channel 7 receptor (P2X7R), an ion channel-type purinergic receptor with adenosine triphosphate (ATP) as its ligand, is widely expressed in various tumor cells, including glioma. Moreover, it plays crucial biological functions in the progression of glioma. P2X7R promotes the proliferation, invasion, and metastasis of glioma by activating multiple signaling pathways, facilitating epithelial–mesenchymal transition (EMT), promoting the release of extracellular vesicles (EVs) and regulating the tumor microenvironment (TME) of glioma. However, the activation of P2X7R by high concentrations of ATP can induce cell necrosis or pyroptosis, exerting an anti-glioma effect. The bidirectional nature of its functions may be related to differences in the subtypes of P2X7R, cell types, as well as the TME. P2X7R antagonists can inhibit its effect in glioma, while the expression of P2X7R can enhance the efficacy of radiotherapy and chemotherapy. In this review, the structure and function of P2X7R, its role in tumor, especially its mechanism of action in glioma, and its latent capacity value as a target for therapeutic of glioma were reviewed in detail.

Empathic pain, a core manifestation of empathy, encompasses an individual's perceptual sensitivity, evaluative judgment, and emotional responsiveness to the suffering of others. This capacity is vital for healthy social interaction, as it fosters prosocial behavior, inhibits aggression, and upholds moral norms critical to social development. This article provides a comprehensive review of current research on empathic pain, examining its conceptual foundations and the underlying neural mechanisms. In particular, it explores the activation of key brain regions, including the anterior cingulate cortex, insula, amygdala, and cerebellum, as well as the neural circuits linking these areas. Additionally, the paper summarizes various influencing factors and modulatory strategies related to empathic pain. These insights enhance our understanding of emotional resonance and establish a solid basis for developing clinical modulation models. Future research should adopt a multidisciplinary approach, incorporating advanced neuroimaging techniques, behavioral experiments, and broader clinical trials to further elucidate empathic pain and inform the development of more effective treatment strategies.

The mechanism of epilepsy is still unclear. We aim to explore the relationship between high-frequency oscillations (HFOs) dynamics and epilepsy, with a focus on deciphering underlying mechanisms at the single-neuron level. Using a rat model of chronic focal cortical epilepsy induced by cobalt-wire implantation, we monitored the seizures and HFO dynamics, as well as the cross-frequency coupling trends between HFOs and theta activities. Additionally, excitatory and inhibitory neurons' discharges were recorded by 16-channel tetrode electrode, with comparisons made between the discharge rates and changes from baselines during different bands of HFOs (ripple:80-200 Hz; fast ripple, FRs:200-500 Hz). All rats (8/8) with cobalt-wire implantation developed spontaneous seizures within 4 to 8 days post-surgery, in contrast to the control group (3/3) with steel-wire insertion remaining seizure-free. HFOs exhibited a progressive increase over time post-surgery in the epilepsy model, while minimal HFOs was observed in the control group. HFOs recorded during the peak-seizure periods showed a propensity to synchronize with the trough of theta activity, coinciding with heightened seizure frequency. A substantial augmentation showed in the discharge rates of both putative excitatory and inhibitory neurons during HFO occurrences. The change ratios between putative excitatory and inhibitory neurons during ripples were smaller than those during FRs. In conclusion, we found that HFO dynamics reflect epileptogenic network formation, with implications for early seizure prediction and therapeutic interventions. Our data provide novel insights at cellular and cross-frequency level into the mechanistic underpinnings of HFO emergence and network reorganization offering potential strategies for targeting pathological network activity in epilepsy.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune condition associated with neuropsychiatric and cognitive deficits. Changes in the cingulate cortex may be central to this disorder. This study investigates subregional alterations in the cingulate cortex of patients with anti-NMDAR encephalitis and their relationship to cognitive deficits using functional and perfusion imaging. Thirty-eight patients with anti-NMDAR encephalitis and 30 healthy controls (HC) underwent resting-state MRI and neuropsychological assessments. We measured low-frequency amplitude (fALFF), degree centrality (DC), and cerebral blood flow (CBF) in the cingulate cortex, and performed functional connectivity (FC) and CBF connectivity analyses. We also analyzed the relationship between subregional changes and cognitive impairment. Finally, we applied support vector machines (SVM) to classify patients and controls based on functional and perfusion features. Patients with anti-NMDAR encephalitis showed significant cognitive impairments in memory and executive function, along with anxiety symptoms. Neuroimaging revealed decreased fALFF, DC, and CBF in the left pregenual anterior cingulate cortex (pgACC.L). FC between pgACC.L and several brain regions, including the parahippocampal gyrus and precuneus, was reduced. Additionally, pgACC.L exhibited altered CBF connectivity patterns with other brain regions. Moreover, the changes of fALFF, DC, and FC are related to the impaired cognitive function of patients. SVM classification based on fALFF, DC, and CBF features successfully distinguished patients from controls. Our findings suggest that pgACC abnormalities play a key role in the pathomechanism of anti-NMDAR encephalitis and may serve as biomarkers for disease monitoring.

Resveratrol is a polyphenol and potent antioxidant that has anti-inflammatory effects in conditions such as atherosclerosis, aortic aneurysm, and inflammatory bowel disease. In this study, we investigated whether resveratrol exerts anti-inflammatory effects and protects against intracranial aneurysm formation and rupture in male mice. Intracranial aneurysms were induced in mice using a combination of elastase injection into the cerebrospinal fluid and deoxycorticosterone acetate-salt (DOCA-salt)-induced hypertension. Male mice were divided into two groups: a resveratrol diet group and a normal diet group. The dietary intervention lasted for 6 weeks, starting 3 weeks prior to elastase injection. The overall incidence of aneurysms did not differ significantly between the normal diet and resveratrol diet groups (71% vs. 59%, p = 0.497). However, resveratrol significantly reduced the rate of aneurysmal rupture compared with that in the normal diet group (88% vs. 40%, p = 0.026). Furthermore, resveratrol supplementation increased the mRNA levels of Sirtuin 1 (Sirt1) and decreased the mRNA levels of nuclear factor kappa B subunit 1 (Nfkb1) and Tumor necrosis factor (Tnf). Our findings demonstrate that resveratrol reduces intracranial aneurysm rupture in a mouse model, indicating its therapeutic potential in this condition.

Tension-type headache (TTH) is a primary headache with the highest prevalence. Previous studies have revealed the local brain abnormalities of TTH patients. However, little is known about its brain connectivity disruption. Based on rs-fMRI data from 33 TTH patients and 30 healthy controls (HCs), static functional connectivity (FC) and dynamic FC were calculated between the default mode network (DMN) and the whole brain. Regions of interest (ROIs)-wise FC was performed to explore the connectivity pattern of the circuit established by the static and dynamic FC methods. The support vector machine (SVM) model was applied to distinguish the TTH patients from HCs. Compared with the HCs, TTH patients showed increased FC between the left posterior cingulate cortex (PCC) and the left parahippocampal and left middle frontal gyrus (MFG). Decreased dynamic FC was observed between the left PCC and right middle occipital gyrus (MOG), left precuneus, left inferior parietal gyrus (IPG), right median cingulate and paracingulate gyri (DCG) and right supplementary motor area (SMA) in TTH patients. The ROI-wise FC results showed that left precuneus-left IPG, left precuneus-right DCG, and left IPG-right SMA generated higher FC in TTH patients. SVM obtained a total accuracy of 70.476%, and the area under the curve (AUC) value was 0.658. TTH patients showed abnormal static and dynamic connectivity in multiple brain regions, and abnormal brain activity was also identified within these brain regions. This novel classification model using the brain connectivity could be useful in detecting neuro-markers for clinical applications in TTH patients.