The cover image is based on the article Real-Time Monitoring of the Antiseizure Drug Valproic Acid Using a Novel Point-Of-Care Mass Spectrometry by Xinqi Fang et al., https://doi.org/10.1111/cns.70499.

Experimental procedures at the animal and cell levels in this study.

PRPF40B promotes circMAN1A2 expression, inhibiting TEP1-KEAP1 complex formation, leading to NRF2 degradation and ferroptosis in GSCs. Without circMAN1A2, NRF2 activation inhibits ferroptosis and promotes TAMs' M2 polarization.

Our study is the first to apply rTMS across five frequency bands to the cerebellum, revealing that low-frequency TMS does not significantly affect working memory. In contrast, 5 Hz rTMS significantly enhances working memory performance and improves the parameters of resting-state brain networks, emphasizing the role of cerebellar rTMS in cognitive regulation.

Mechanistic model of EA-ST36-mediated reversal of HFD-induced cognitive impairment in 3xTg-AD mice through TFEB/TFE3 activation. The model illustrates that EA-ST36 inhibits MTORC1 and activates TFEB/TFE3, enhancing the autophagy-lysosomal pathway (ALP), which leads to the effective degradation of Tau aggregates and NLRP3 inflammasome components in the hippocampi of HFD-fed 3xTg-AD mice.

This study reveals two distinct neuroanatomical subtypes of fibromyalgia. Differences in clinical symptoms and treatment responses between two subtypes validate the subtype classification and highlight variations in the underlying neuropathological processes of fibromyalgia, offering insights for individualized treatment strategies.

This meta-analysis systematically evaluated the effectiveness of oropharyngeal sensory stimulation in managing ND, demonstrating significant improvements in swallowing function and decannulation rates. While electrical stimulation exhibited consistent therapeutic benefits, the clinical implications of gustatory stimulation remain inconclusive and warrant further investigation.

Chronic hyperglycemia disrupts the cystine/SLC7A11/glutathione axis, impairing cystine uptake and depleting glutathione in dopaminergic neurons, increasing ferroptosis susceptibility. SLC7A11 restoration rescues neuronal viability, restores redox balance, and attenuates neurodegeneration in diabetic PD models. SLC7A11 emerges as a therapeutic target to mitigate PD risk in diabetic individuals.

Our results point to the importance of the WWI in predicting the risk of depression in middle-aged and older adults. In future intervention wording, WWI may become a target to reduce the high prevalence of depression in middle-aged and older adults. Image was created in BioRender. Liu, G. (2024) https://BioRender.com/e47a501.

We present a novel point-of-care mass spectrometry system enabling rapid, real-time quantification of valproic acid directly from whole blood. This bedside platform delivers serum-equivalent results within 3 min and captures pharmacokinetic variability perioperatively, supporting individualized antiseizure therapy and timely clinical decision-making in neurosurgical patients.

A novel minimally invasive surgical approach, the isthmic approach, was introduced for the treatment of thoracic extradural schwannomas. A retrospective analysis of 41 clinical cases demonstrated that this approach improves total tumor resection rates, preserves spinal stability, and significantly reduces operative time, incision length, and intraoperative blood loss.

Dehydrocostus lactone (DHC) inhibits microglia-mediated neuroinflammation by targeting CYP2A6, reducing the release of pro-inflammatory factors and improving nerve function impairment, thereby alleviating ischemic brain injury.

Microglia interact with oxidative stress, reactive astrocytes, neuronal damage, neuroinflammation, synaptic dysfunction, mitochondrial dysfunction, epigenetic modifications, and blood–brain barrier disruption, playing a critical role in the pathophysiology of perioperative neurocognitive disorders (PND). Targeting microglia presents a promising therapeutic strategy for the management of PND.

rTMS inhibits clinical seizure and decreases SWI. rTMS improves cognitive function. rTMS increases in the sleep spindle and the sleep spindle coupling in the slow wave up-state. rTMS improves cognitive function via increases of the sleep spindle.

Diagram of findings: Surgical trauma is a major contributor to postoperative delirium, inflammation, and neuronal injury. Low body temperature at the end of surgery may be a risk factor for postoperative delirium in patients with open surgery repair for thoracic aortic aneurysm.

Schematic diagram of the role and activation mechanism of GABAergic neuron pyroptosis in CPSP. Downregulation of Mfn2 induces the GABAergic neuron pyroptosis which is involved in the development of chronic postoperative pain by promoting mitochondrial dysfunction and ROS accumulation.

Social isolation exacerbates anxiety, depression, and social cognitive deficits in early-stage AD mice by disrupting the oxytocin system, while intranasal oxytocin mitigates behavioral abnormalities, reduces pathological damage, and restores gut microbiota homeostasis.

This integrative genetic study, using Mendelian randomization and transcriptome-wide association analyses, demonstrates that birth weight decreases functional connectivity of the central executive or default mode network in the temporal lobe, childhood BMI reduces connectivity in subcortical-cerebellum and motor/attention networks, and adulthood BMI increases neural activity in the frontal lobe.

Chronic stroke patients exhibit persistent glymphatic dysfunction (reduced DTI-ALPS index), with lesioned hemispheres showing greater impairment at 3 months post-stroke. Partial functional recovery occurs by 1 year, resolving interhemispheric differences. Transient weak correlations between ALPS index and motor/memory scores at 3 months disappear at 1 year, indicating stabilized recovery patterns. Lesion location and volume show no significant impact. These findings validate DTI-ALPS for chronic-phase monitoring and highlight glymphatic restoration as a therapeutic target for PSCI.

Multi-technology interventions (non-invasive neuromodulation, AI, 3D organoids) for CNS tumor treatment shift from monotherapy to functional reconstruction. They address BBB restriction, tumor heterogeneity, and immune suppression via biological–psychological–technological convergence, enabling precision oncology through dynamic monitoring and microenvironment remodeling. Despite translational/ethical challenges, interdisciplinary innovation drives patient-centered functional restoration.

This study explored the effects of LILRB4 on PD by analyzing the association between LILRB4 and PD clinical characteristics and hallmarks. LILRB4 might be vital in gatekeeping PD clinical characteristics by tuning nigrostriatal dopaminergic neuron function, AD-related pathology, WM microstructural alteration, and astrocyte activation.

The study explores the impact of maternal diabetes on neonatal brain development, revealing significant weight reductions and alterations in brain structure, suggesting potential neurodevelopmental consequences and insulin treatment benefits.

Higher estimated glucose disposal rate (eGDR) may be linked to improved cognitive function and reduced risk of cognitive impairment in older adults. eGDR outperforms other insulin resistance indices, highlighting its potential as a predictive marker for cognitive health, with machine learning models confirming its clinical utility.

Diagram of the mechanism underlying the effect of EA-CV23 treatment on PSD. Excitatory neurons in the VPM are required for EA-CV23 mediated alleviation of swallowing dysfunction in PSD model mice. This modulatory effect of EA involves the NTS-VPM-S1 neural circuit.

The classification model based on ¹⁸F-FDG PET and scalp EEG brain network features effectively identifies TPE patients with insular involvement from TLE patients. There are differences in the local network features of the insular region between the two patient groups.

This study examines glymphatic dysfunction in pDoC via BOLD-CSF coupling analysis using MRI. pDoC patients show delayed time-lags and reduced coupling strengths, with time-lags predicting consciousness recovery. Findings suggest glymphatic dysfunction as a potential biomarker for consciousness recovery in pDoC.

Dual-target iTBS promotes neural regeneration and synaptic reconstruction after SCI via the PDE1A/cAMP/PKA signaling pathway. Inhibiting PDE1A promotes neural growth and synaptic function.

PD-L1 plays a critical role in ischemic stroke recovery, with PD-L1 mAb treatment demonstrating age-dependent therapeutic efficacy by enhancing blood–brain barrier integrity, reducing neuroinflammation and apoptosis, and modulating peripheral immune responses.

Impaired autophagy in Alzheimer's disease leads to accumulation of amyloid-β and tau aggregates, while senescent brain cells secrete pro-inflammatory SASP factors. The interplay between defective clearance and chronic inflammation accelerates neuronal dysfunction and highlights autophagy enhancers and senolytics as promising therapeutic strategies.

High-expressed NFE2L1 contributes to maintaining the M2 macrophage in glioma. Knockout of NFE2L1/Nrf1 can reverse the M2 phenotype of TAMs to the M1 phenotype. In vivo tumor growth is significantly inhibited in NFE2L1^−/+-deficient heterogeneous mice. The activity of CD38 and PDL-1 inhibitors is enhanced by NFE2L1 targeting the ARE sites. The anti-PD-1 therapeutic efficacy is strikingly enhanced on NFE2L1^−/+ tumor-bearing mice.

Knockdown of Ptbp1 in spinal cord astrocytes promotes motor function recovery after sciatic nerve injury by inducing their transdifferentiation into motor neurons and polarization toward the neuroprotective A2 phenotype. Concurrently, Ptbp1 depletion in dorsal root ganglion satellite glial cells enhances sensory axon regeneration through the activation of the ntng2/NGL-2 signaling pathway.

Our findings reveal a causal effect of large clone clonal hematopoiesis (CH) on cardioembolic stroke (CES). PARP1 and CD3G were identified as key genes linking CH to CES. Using 113 machine learning algorithm combinations, we pinpointed 14 feature genes that played critical roles in the pathway from CH to CES, a finding further validated by eQTL, pQTL, and summary-data-based Mendelian randomization (SMR). Additionally, we integrated bulk RNA and single-cell RNA sequencing analyses to explore the underlying mechanisms of this association.

Using a clinical cohort of 429 patients, this study identified age-related carotid anatomical changes—such as increased tortuosity, arterial stiffness, and CCA diameter variation—that were significantly associated with CAS/CEA complications. A logistic regression model accurately predicted CAS complications (AUC = 0.82), outperforming multiple machine learning methods. Findings may aid in optimizing patient selection and surgical planning in the elderly.

This review summarizes that albiflorin alleviates depression by modulating neuroinflammation and enhancing neurotrophic signaling. Following oral administration, albiflorin crosses the blood-brain barrier and acts primarily on the hippocampus and prefrontal cortex. It suppresses microglial activation and reduces the expression of pro-inflammatory cytokines such as IL-1β and TNF-α. At the same time, albiflorin promotes the expression of brain-derived neurotrophic factor (BDNF) through the activation of key signaling pathways, including PI3K/Akt, MEK/ERK, and cAMP/PKA. These molecular effects contribute to neuronal repair, restoration of synaptic plasticity, and the mitigation of depressive-like behaviors. Altogether, the findings highlight the multi-target mechanisms through which albiflorin exerts its antidepressant effects, supporting its promise as a potential therapeutic agent for neuropsychiatric disorders.

AD16 regulates M1/M2 microglia polarization by α7nAChR–ERK–STAT3 signaling to restrain neuroinflammation induced by ischemic stroke.