Glioma is the most prevalent primary central nervous system malignant tumor, with high heterogeneity observed among different grades; therefore, non-invasive prediction of prognosis could improve the clinical management of patients with glioma. ¹H-magnetic resonance spectroscopy (MRS) can estimate metabolite levels non-invasively. Multiple studies have investigated its prognostic value in gliomas; however, no consensus has been reached. PubMed and Embase databases were searched up to 20 October 2022 to identify studies investigating the prognostic value of metabolites using ¹H-MRS in patients with glioma. Heterogeneity across studies was evaluated using the Q and I² tests, and a fixed- or random-effects model was used to estimate the combined overall hazard ratio (HR). Funnel plots and Begg tests were used to assess publication bias. Higher choline levels were associated with shorter overall survival (HR = 2.69, 95% CI, 1.92–2.99; p < 0.001) and progression-free survival (HR = 2.20, 95% CI, 1.16–4.17; p = 0.02) in all patients; however, in pediatric gliomas, it showed no significant correlation with overall survival (HR = 1.60, 95% CI, 0.97–2.64; p = 0.06). The estimated choline level by ¹H-MRS could be used to non-invasively predict the prognosis of patients with adult gliomas, and more studies are needed to evaluate the prognostic value of other metabolites.

Temozolomide (TMZ) resistance remains a major clinical obstacle in the treatment of glioblastoma (GBM), a highly aggressive brain tumor with poor prognosis. Growing evidence showed that metabolic reprogramming contributed to TMZ resistance and offered new avenues for intervention. This review comprehensively summarizes resistance-associated changes across three key areas – glycolysis, redox homeostasis, and lipid metabolism in TMZ-resistant GBM. The resistant cells tend to display enhanced glycolytic flux, with upregulation of glucose transporter and glycolysis enzymes. To counteract TMZ-induced oxidative stress, antioxidant systems are activated. Lipid metabolism is also extensively rewired, involving increased fatty acid oxidation, de novo lipogenesis, steroid hormone synthesis, and prostaglandin E₂-mediated signaling, along with a decreased ceramide level. Emerging preclinical research investigated therapeutic strategies targeting resistance-associated metabolic changes to reverse TMZ efficacy. Though preclinical research showed encouraging results, further validation in clinical settings is still needed. A deeper understanding of context-specific metabolic adaptations helps better elucidate the role of metabolism in resistance and to identify therapeutic opportunities with greater clinical translational potential.

The efficient establishment of in vitro neural models that accurately mimic the structural and functional connectivity of neural networks is critical in neuroscience research. 3D bioprinting shows great potential for constructing sophisticated in vitro models with high freedom of design. However, mature neurons are delicate and susceptible to manipulation. Here, extrusion‐based 3D bioprinting is employed to fabricate gelatin methacryloyl (GelMA)‐based constructs containing embryonic day 18 (E18) rat cortical neurons, referred to as 3D neuMatrix. 3D neuMatrix displays favorable neuronal viability, with the progressive formation of a 3D brain‐like neural network with local and long‐range functional axon connections. Compared with 2D cultured neurons, 3D neuMatrix is more similar to the E18 cortex according to the bulk transcriptomic profile, with a recreation of cellular components in the cerebral cortex. The 3D neuMatrix is employed to establish a disease model of ischemic stroke, with a faithful recapitulation of the viability, function, and transcriptomic features of rats with middle cerebral artery occlusion/reperfusion (MCAO/R). These findings demonstrate the formation of multiscale neural circuits within 3D neuMatrix and its valuable potential in the study of neurodevelopment, disease modeling with drug screening, and in vitro intelligence.

This study aimed to investigate the therapeutic effects and neural mechanisms of high-frequency neuro-navigated repetitive transcranial magnetic stimulation (nrTMS) targeting the hand knob in glioma patients with postoperative motor deficits, using functional gradient analysis to characterize cortical reorganization. Thirty patients with postoperative motor deficits were randomized to receive nrTMS or sham stimulation targeting the ipsilateral hand knob. Motor function was assessed using Fugl-Meyer Assessment (FMA) and muscle strength. Resting-state fMRI was acquired to compute principal functional gradients. Control/tumor, nrTMS/sham, and Pre-TMS/Post-TMS gradient changes were analyzed. Correlation and regression analyses related to motor recovery were performed. The nrTMS group showed significantly greater improvement in muscle strength (Post-treatment: nrTMS: 3.533 ± 0.720, Sham: 2.067 ± 0.572, p = 0.019, d = 1.082; 3-month follow-up: nrTMS: 4.600 ± 0.408, Sham: 3.733 ± 0.609, p = 0.035, d = 1.012). Gradient analysis revealed increased sensorimotor network (SMN) gradient scores following nrTMS (Pre-TMS: -0.707 ± 0.108; Post-TMS: -0.636 ± 0.077; p = 0.016), and HH_SomMot_22 within upper limb motor cortex is most strongly correlated with motor recovery. High-frequency nrTMS targeting the hand knob accelerated the motor recovery. Gradient analysis findings provide novel insights into therapeutic mechanisms of nrTMS and underscore the value of the hand knob as a stimulation target.

Meningiomas are the most common primary intracranial tumors of the central nervous system. They exhibit highly heterogeneous biological behavior that current histological grading cannot reliably predict. Currently, there are no standardized systemic treatment regimens for recurrent or refractory meningiomas; therefore, molecular subtyping is crucial for assessing prognosis and guiding treatment decisions. Key alterations, including NF2, TERT promoter, CDKN2A/B, AKT1, and SMO, contribute to the proliferation, invasion, and recurrence of meningiomas. This review summarizes the advances in molecular pathological alterations and clinical studies on systemic therapy for meningiomas. Anti-angiogenic agents, immune checkpoint inhibitors, and inhibitors targeting multiple signaling pathways represent promising directions. Anti-angiogenic therapy has demonstrated disease control, whereas PD-1 inhibitors have shown limited benefit in unstratified populations but may be of value in specific molecular subgroups. Molecularly stratified umbrella and basket trials are advancing precision treatment, and peptide receptor radionuclide therapy provides benefit for patients with specific molecular alterations. Some early trials of targeted therapies and immunotherapies have shown positive signals, but the overall level of evidence remains limited. Future studies should employ more rigorous trial designs and encourage patient participation to clarify the clinical value of each strategy and drive the shift from empirical to molecularly guided treatment.