Cover image: The cover image is based on the article High-Frequency rTMS Improves Visual Working Memory in Patients With aMCI: A Cognitive Neural Mechanism Study by Yun-Xia Li et al., https://doi.org/10.1111/cns.70301.

Cover image: The cover image is based on the article Electroacupuncture Regulates Sympathetic Nerve Through the NTSGlu–RVLM Circuit to Relieve Spontaneous Pain in SNI Rats by Wen Chen et al., https://doi.org/10.1111/cns.70327.

Acute poisoning with the organophosphate, soman, triggers status epilepticus that rapidly becomes refractory to standard of care treatment with midazolam (MDZ). Combined treatment with MDZ and allopregnanolone (ALLO) significantly suppresses seizure activity, which is associated with attenuated neurodegeneration and neuroinflammation.

The Role of TCD in Assessing Postoperative Collateral Development and Long-Term Clinical Outcome in Moyamoya Disease.

Acupuncture improves cognitive dysfunction caused by chronic cerebral ischemia by regulating the CKLF1/HIF-1α/VEGF/Notch1 pathway to increase cerebral blood flow.

CS15-GNPs exhibited favorable neuroprotection and biosafety. This study develops an innovative ApoE-mimetic peptide-capped GNPs, which provides a potential strategy for the treatment of ischemic stroke.

An average propofol infusion rate ≥ 20 μg/(kg*h) during the initial 18 h of IMV was identified as an independent risk factor for postoperative delirium. This finding was further supported by subgroup analyses.

The identification of rs1399178 as a bifunctional regulatory element, mediating promoter-enhancer switch and interacting with NRF1, sheds light on the complex regulatory networks involved in schizophrenia pathogenesis.

It is the first study to link nonmotor symptoms with falls in Parkinson's patients post-DBS. Generalized estimating equations were used to assess the longitudinal impact of NMS with falls in 136 patients, finding that mood/cognition, gastrointestinal, and urinary symptoms, as well as their interactions with motor symptoms, were related to fall risk.

A structural connection between the pancreas and the brain was established and identified the mechanisms through which the lateral parabrachial nucleus (LPB) modulates chronic pancreatitis pain.

This graphical abstract synthesizes a comprehensive ADHD study, showcasing how combining qEEG and TOVA metrics with demographic data through ALM can enhance diagnostic accuracy, particularly emphasizing the significant inverse relationship between age and theta/beta ratios in ADHD symptomatology.

Carotid PET/MR-related indicators (high PET uptake, high SCAIL scores, AHA VI type plaques) can effectively predict the risk of new ischemic lesions after carotid artery stenting, aiding in the early identification of high-risk patients for recurrent ischemic stroke.

This study demonstrates that compared to APOE3, APOE4 exacerbates Aβ deposition, microglial activation, and synaptic degeneration in the presymptomatic stage of 5xFAD mice. Proteomics and phosphoproteomics reveal the potential mitochondrial mechanisms by which APOE4 promotes synaptic degeneration.

Does magnetic shock have an impact on the brain? No, it is effective and safe! Magnetic shock therapy (MST) has significant advantages in treatment. After the patient was admitted, the doctor recommended more advanced magnetic shock therapy to her, which caused less damage to the brain's cognition and memory. The focus of this project is to explore the effect of magnetic shock on the thickness of the cerebral cortex.

Knockdown of SESN2 in MCAO mice increased the expression of the p-mTOR/HIF-1α pathway, which increased glycolysis and lactate levels and, in turn, affected IS injury.

MT has a positive effect on dynamic cerebral autoregulation (dCA) at the acute phase of stroke. For MT patients, dCA is a reliable indicator for predicting the prognosis of patients and may be an intervention target to improve outcomes.

A diagram illustrating a network-based mechanism exploration framework for XBP against brain injury after cardiopulmonary resuscitation. (A) In vivo and in vitro pharmacodynamic confirmation of XBP against PBI. (B) Network pharmacology approach as well as metabolomics analysis to explore the potential mechanisms. (C) Mechanism verification of XBP against PBI.

The article unraveled that preventive administration of DNLA may delay the impairment of learning and memory in APP/PS1 mice. The molecular mechanism may be related to promoting the mTOR-TFEB-v-ATPase pathway.

Through the use of a combined retrospective and prospective study, vWF might be a novel blood biomarker for predicting s-HT occurrence in ischemic stroke patients.

The effect of gut-brain axis lipid abnormalities metabolism mediated by circadian rhythm disruption on AD were discussed. The membrane lipids abnormalities surrounding sarcoplasmic reticulum Ca²⁺ -ATPase (SERCA) influencing SERCA to release Ca²⁺ mediate ERS and inflammation, which contribute to neuron damage Aβ accumulation in AD. In addition, Intestinal mucosal ERS leads to increased permeability, and accelerate AD progression by the increase of Lipopolysaccharide and proinflammatory factor.

We investigated the metabolic alterations resulting from ketamine administration. Ketamine alters mitochondrial function, increases ATP/ADP, impacts BDNF in responders, and lower baseline FT3 is associated with greater MADRS reduction in ketamine treatment.

Central thalamus deep brain stimulation (DBS) exerts a regulatory effect on the autonomic nervous system in patients with disorders of consciousness (DOC). We analyzed the HRV indices, including time-domain and frequency-domain parameters across various time points for all patients. The HRV exhibited a consistent trend across the three groups with different parameters. Notably, the most pronounced HRV changes were induced by the 100 Hz. Long-term follow-up indicates that high-frequency (HF), low-frequency (LF), and total power (TP) of HRV may serve as predictive indicators in the prognosis of patients.

A. muciniphila may regulate neuroinflammation and cognitive impairment via hippocampal NLRP3-mediated neuroinflammation, and the peripheral T cell response might modulate the relationship between intestinal microbiota and cognitive behavior.

SEEG plays a crucial role in pediatric epilepsy surgery, particularly in children under 6 years old. Total resection with lesional MRI and FCD type II was the most favorable prognostic predictor for achieving seizure freedom in children undergoing SEEG-guided surgery.

Our study revealed significant disruptions in brain structural networks in vascular cognitive impairment participants, including reduced fractional anisotropy and altered network properties. Despite no significant functional topology differences, enhanced structure–function coupling in key regions correlated with cognitive performance, suggesting compensatory neuroplasticity and offering insights for cognitive disorders prevention.

Our study found that MDD caused a decrease in CT in the medial orbitofrontal region, a decrease in SA in the paracentral region, and an increase in SA in the lateral occipital region.

Anwulignan enhances PPARα expression in the spinal dorsal horn of rats, facilitating its binding to RXR and forming an active PPARα/RXR complex. This complex translocates to the nucleus, inhibits CXCR2 expression, and alleviates bone cancer pain (BCP) while reducing tumor-induced bone destruction and burden.

We successfully identified specific biomarkers associated with stroke mechanisms. We developed a methodology that enabled the identification of biomarkers for different stroke subtypes, such as cardioembolism, large artery atherosclerosis, and cancer-related, through proteomic analysis.

Effect of EA on the NTS^Glu-RVLM circuit in the regulation of sympathetic nerve activity in SNI rats.

Our work explores the role of protein posttranslational modifications (PTMs) in glioma. Through the screening of PTM pathways and the analysis of related molecular characteristics, we identified prognosis-related genes and evaluated and constructed PTM-related prognostic signatures.

Schematic diagram of potential mechanisms by which SIK2 regulates autophagy in ALS. SIK2 contributes to the induction of autophagy by inhibiting mTORC1 signaling. However, SIK2 disrupts lysosomal dysfunction, ultimately resulting in defective autophagy flux. Inhibition of SIK2 promotes mSOD1 accumulation removal by activating autophagy flux and restores mTORC1 activity, thus playing a neuroprotective role on motor neurons in ALS.

We found a significant interaction effect between group and condition in the right dorsolateral prefrontal cortex. Bonferroni post hoc tests indicated MSA-P patients exhibited a significant increase in ΔHbO₂ compared to PD patients during the DTW condition.

In children with SeLECTS, early EEG features such as SWF, relative PSD, wPLI, and CPL are significantly associated with the presence of EE-SWAS during the disease course. We successfully construct a model to predict the evolution of EE-SWAS in SeLECTS, thereby aiding early clinical diagnosis and timely intervention for EE-SWAS.

The present result suggests that a sizeable portion of the population has inefficacious activity in the setting of certain antiplatelet agents. Additionally, sex and ethnicity differences in responsiveness to aspirin or clopidogrel have been noted.

Study design comparing the treatment and sham groups. The treatment group received 4 weeks of rTMS on the DLPFC (5 days per week), while the sham group underwent sham stimulation. Assessments were conducted at baseline (T0), 4 weeks (T1), 3 months (T2), 6 months (T3), and 12 months (T4), measuring ECAS, Zarit, ALSFRS-R scores, and NF-L levels to evaluate group differences.

Based on prospective observations of the characteristics of post-radiosurgery headache, supplementary diagnostic criteria have been proposed. Female gender, younger age, no prior craniocerebral surgery, and multiple lesions are identified as risk factors for the occurrence of post-radiosurgery headache.

Acute restraint stress regulates ATP production in the hippocampus of Alzheimer's disease model mice and inhibits abnormal activation of AMPK under the pathologic condition, resulting in the removal of the suppression of the mTOR pathway, which is involved in the enhancement and maintenance of L-LTP.

Located beyond the tumor core, questiona cells (Q cells) exhibit high invasiveness, metabolic adaptations, and drug resistance, driving tumor recurrence despite aggressive treatment. Their physical properties, such as low solid stress and soft tissue stiffness, further enhance their migratory and invasive capabilities. Advanced imaging techniques (e.g., DTI, MRS, DWI, PET) enable their detection, while interactions with the tumor microenvironment (e.g., TAMs, Tregs, fibroblasts) present new therapeutic challenges and opportunities.

Gastrodin reduces tau hyperphosphorylation in 3xTg-AD mice, reverses decreased brain matrix viscoelasticity, and remodels ECM components by targeting the Alzheimer's risk gene FERMT2, primarily in astrocytes. It binds to FERMT2, inhibiting its expression, which leads to ECM remodeling, restored matrix viscoelasticity, and blood–brain barrier recovery. Gastrodin also modifies neuroinflammatory factors such as TNF-α, IL-6, and MMP8.

R13 blocks the activation of AEP to prevent delayed tPA-induced hemorrhagic transformation after ischemic stroke.

Phytol (PHY) concentration-dependently inhibited GABA activity and dose-dependently reduced immobility time (IMT) in Swiss mice. It also modulated the GABA activity and IMT values of diazepam and flumazenil. It showed a slight sex-dependent antidepressant effect on mice, possibly through the GABAA receptor interaction pathway.

QO-83 has better opening effects on K_V7.2 and K_V7.2/7.3 channels, with W236 as the key site for its high binding free energy to K_V7.2. By opening K_V7 channels, regulating sIPSC and sEPSC amplitudes, and inhibiting epileptiform discharges, QO-83 outperforms RTG in both acute and chronic epilepsy models.

AE activates the AMPK/PGC-1α/SIRT3 pathway. Increased expression of SIRT3 in mitochondria promotes mitophagy and regulates the function of mitochondrial proteins. Consequently, the mitochondrial membrane potential, GSH, ROS, and Ca²⁺ levels gradually recover, alleviating the pathological manifestations of ad.

Prenatal stress increases the risk of neurodevelopmental disorders and psychiatric illnesses in offspring. This study demonstrates that melatonin alleviates emotional and cognitive deficits in offspring exposed to prenatal stress. By modulating the PI3K/AKT/NF-κB signaling pathway in microglia and reducing the elevated expression of CXCL10 in the dentate gyrus, melatonin promotes neurogenesis and synaptic plasticity.

NP induces LC neuron loss; it also diminishes norepinephrine (NE) release and increases inflammatory activation of microglia and neuroinflammation in CA3 of the hippocampus. Selective activation of the LC-CA3 noradrenergic neurons with Gq-DREADD efficiently alleviates NP and anxiety- and depression-like behaviors, and reduces microglial neuroinflammation in CA3 of mice 12 weeks post-SNI.

TSG-6 diminishes infarct volume, enhances neurological function, and mitigates blood–brain barrier damage following acute cerebral ischemia–reperfusion injury. Furthermore, TSG-6 exerts neuroprotective effects by upregulating Hsp70-1B to inhibit NF-κB phosphorylation in oxygen–glucose deprivation/reoxygenation-induced astrocytes, thereby suppressing apoptosis, astrocyte reactivity, and A1 phenotype transformation.

We developed a novel nomogram that incorporated four routine clinical variables with two OCTA-derived retinal microvascular metrics in predicting END in SSI patients, which exhibits high accuracy in predicting END in SSI patients. It could help identify SSI patients with a high risk of END at an early stage and benefit a better prognosis.

Downregulation of MeCP2 targeted by miR-199-3p in the hippocampal neural stem cells of mice with chronic neuropathic pain induces inhibition of adult neurogenesis, thus leading to depression-like behaviors.

H₂S promotes neuron survival and motor functional recovery via inhibiting neuronal ferritinophagy-mediated ferroptosis induced by spinal cord ischemic-reperfusion injury.

Nigrostriatal iron gradients are similar in HC, PD, and MSA, with variation in extent. Iron deposition in the SN emerged as a consistent feature in synucleinopathies. MSA has a higher iron content in the posterolateral putamen compared to PD.

We investigated the relationship between brain iron levels, emotion, and cognitive and motor function in cerebral small vessel disease (CSVD) patients using quantitative susceptibility mapping (QSM). Our findings showed that increased brain iron levels were significantly associated with anxiety and motor dysfunction in CSVD patients. Iron deposition may disrupt normal brain function by inducing oxidative stress and neural damage, worsening cognitive and motor symptoms. These results suggest that brain iron levels could serve as a biomarker for neurological symptoms in CSVD and potential therapeutic targets for future treatments.

A cohort of 340 AIS patients treated with rt-PA thrombolysis was analyzed. BP at 39 time points showed significant disparities in 24-h post-thrombolysis systolic BP between mRS 0–2 and mRS 3–6 groups, with lower systolic BP indicating better 90-day functional outcomes.

Extending the treatment duration of minocycline appropriately can more effectively inhibit neuroinflammatory injury caused by microglial activation in stroke. In the process, glycolysis levels were downregulated through the EMB/MCT4/STING axis, thereby suppressing neuroinflammatory responses induced by microglia.

This study used meta-analysis to establish a correlation between low UA levels and MG. Furthermore, MR and bioinformatics analyses identified IGF1R as a key protein in this relationship. The correlation between IGF1R and MG was further validated using the TCGA dataset, GEO single-cell RNA sequencing datasets, and clinical data from MG patients, which indicated that low IGF1R expression is associated with MG. Finally, several small-molecule drugs targeting IGF1R were identified, offering potential therapeutic options for MG.

Post-COVID-19 neurological syndrome, marked by cognitive dysfunction, stems from mechanisms like neuroinflammation, cerebrovascular injury, and psychological stress. This review highlights pharmacological treatments and cognitive rehabilitation as promising strategies to address cognitive impairment from acute COVID-19 to long-COVID phases.