Cover image: The cover image is based on the article Theta Rhythm-Based Attention Switch Training Effectively Modified Negative Attentional Bias by Yifeng Wang et al., https://doi.org/10.1111/cns.70157.

The authors propose an approach for CM-targeting individual TMS, using two group clusters of left and right CM which were functionally connected with the left primary sensorimotor cortex (PSMC) and the right superior of frontal gyrus (SFG) in the RS-fMRI analysis.

CCN1-S100A8 pathway is important for the MES phenotype transition. FAK/STAT3 and NF-κB/p65 signaling participated in CCN1/S100A8-mediated MES phenotype transition in GSCs.

This single-center retrospective cohort study indicates that the triglyceride-glucose index (TyG index), as a marker of insulin resistance, was significantly linked to worse functional outcome, increased mortality at 90 days, and a higher risk of symptomatic intracranial hemorrhage (sICH) in patients with acute ischemic stroke postendovascular treatment. In addition, the TyG index was not significantly associated with early neurological deterioration (END).

Hyperlipidemia is a common comorbidity of stroke, which exacerbated ischemic brain injury. We found that hyperlipidemia promoted alternative splicing of Cflar_R via upregulating Mef2c expression in ischemic neurons, thus aggravated neuron necroptosis and neurological deficits following ischemic stroke. This pathogenic splicing process is a promising target for hyperlipidemic stroke patients.

Surgery combined with perioperative sleep deprivation induces decreased GDNF in the lateral basal forebrain, which leads to enhanced apoptosis and autophagy dysfunction of cholinergic neurons and increased risk of chronic postsurgical pain. Normalizing GDNF levels by AAV-GDNF therapy rescues the deleterious effects of perioperative sleep deprivation. Selective lesion of the cholinergic neurons of lateral basal forebrain by mu p75-SAP decreases the pain threshold and abolishes the pain-enhancing effects of sleep deprivation.

Rg1 exhibits antidepressant effects through diverse mechanisms, such as anti-inflammation, synaptic protection, neurogenesis promotion, brain-derived neurotrophic factor release, enhancement of astrocyte gap junction function, and regulation of hypothalamic–pituitary–adrenal axis and antioxidative stress. Experimental studies validate Rg1's efficacy in depression treatment, with molecular docking analysis supporting its promising application prospects.

Susceptibility-ALFF may serve as a valuable biomarker for early assessment of cognitive decline in CKD, offering insights into the pathogenesis of cognitive decline in CKD. HC, healthy control; ALFF, amplitude of low-frequency fluctuations; ReHo, regional homogeneity; CBF, cerebral blood flow; ROI, region of interest.

Bmal1 regulates the pyroptosis pathway after spinal cord injury. Bmal1 inhibits the NF-κB/MMP9 signaling pathway, reduces inflammatory response, and ultimately inhibits pyroptosis in mice spinal cord injury models.

A novel indicator combining NAR and TG is positively associated with sHT in AIS patients. The constructed nomogram, integrating this novel indicator with other risk factors, provides a valuable tool for identifying sHT risk, aiding in clinical decision-making.

The underlying mechanism of oral–gut–brain axis between periodontitis and ischemic stroke could occur through the following pathways: (1) direct transfer of bacteria and their products via nervous or blood; (2) gut dysbiosis due to imbalanced oral microbiota; and (3) activation of inflammatory and immune responses activation by the secretion of inflammatory mediators.

Brain-derived neurotrophic factor (BDNF) is not only the main neurotrophic signal in the human body but also an important neuromodulator. BDNF and its receptors are widely distributed throughout the central nervous system. They promote neuronal survival and growth and protect neurons. They are considered to be the guiding mediators of central nervous system functional and structural plasticity. Reduced BDNF levels in the central and peripheral systems are closely related to various neurological diseases, including neuropathic pain, inflammatory pain, and mental illness. More and more studies have shown that BDNF can potentially increase the growth, survival, proliferation, and migration of cancer cells, affecting cancer development. When BDNF and its receptor tropomyosin receptor kinase B are missing in the signaling pathway, brain and cardiovascular diseases are also more likely to occur. This article focuses on summarizing and analyzing the effects of BDNF on neurological diseases, cancer, and cardiovascular diseases to clarify its effects on these diseases and provide new ideas and methods for the treatment of these diseases.

After stroke, macrophages and microglia transition from an anti-inflammatory to a proinflammatory phenotype due to lysosomal overload and impaired STING degradation. The activation of STING and the subsequent type I interferon signaling pathways results in the phenotypic transition of macrophages/microglia. Inhibiting STING can reverse the proinflammatory shift, thereby reducing poststroke neural inflammation and improving neurological outcomes.

After aneurysmal subarachnoid hemorrhage, the cerebral autoregulation is destroyed, and the cerebral blood flow is dependent on blood pressure. Reliable recommendations on periprocedural blood pressure target are still lacking and remains inconclusive. This study aimed to investigate the association between intraoperative hypotension and newly developed cerebral infarction.

tPBM employs red or near-infrared light to enhance mitochondrial function, promote neurogenesis, and reduce neuroinflammation, offering potential benefits for stroke recovery. This review summarizes evidence from animal studies and clinical trials validating tPBM's efficacy and discusses translational challenges and future directions in treatment advancement.

This real-world study revealed substantial clinical overlap between MMD and MMS. Both groups derived significant benefits from surgical revascularization, suggesting distinction may not be necessary to guide surgical management decisions. Optimizing preoperative status and preventing periprocedural complications may improve outcomes in these rare cerebrovascular conditions.

Pleiotrophin (PTN) overexpression reduces adolescent ethanol consumption, prevents ethanol-induced microglial activation, and alters hippocampal neurogenesis and PNNs remodeling, highlighting PTN's role in alcohol-induced brain alterations.

Brain-derived neurotrophic factor (BDNF) is crucial for neuronal survival and plasticity in the CNS, acting through NTRK2/TRKB receptors. It also plays a role in inhibiting microglial activation and pro-inflammatory cytokine release. This review examines the controversial BDNF levels in multiple sclerosis (MS) stages and explores how BDNF signaling and its modulators influence MS pathogenesis and outcomes.

The anti-inflammatory and neuroprotective mechanisms of the novel drug LIGc in models of neuroinflammation and cerebral ischemic injury involve its ability to downregulate the expression of the FPR1/NLRP3 signaling pathway in microglia/macrophages. This regulation facilitates the transformation of these cells into an anti-inflammatory phenotype, leading to inhibition of pro-inflammatory factor release and promotion of anti-inflammatory factor production.

Administering caffeine preventively to mice can alleviate memory deficits caused by hypobaric hypoxia conditions. The possible mechanism is that caffeine inhibits A₂A receptors, thereby promoting the expression of tyrosine hydroxylase, which in turn affects the release of dopamine and dopamine metabolism.

A comprehensive analysis of the large-scale real-world FAERS database was conducted to evaluate the relationship between SNRIs and adverse reproductive system events. In patients treated with SNRIs, males should focus on erectile dysfunction and retrograde ejaculation, while females should be alert to potential associations with ovarian cysts.

Inhibitors of the NLRP3 inflammasome activation pathway for the treatment of MS (Created with BioRender).

Preterm white matter injury (PWMI) is the most common type of brain injury in preterm infants. In this study, human OPCs (hOPCs) were administered to a fetal goat model of PWMI. Exogenous hOPCs can differentiate into mature oligodendrocytes in fetal goats and alleviate hypoxia-ischemia-induced PWMI.

BPPV patients with RD showed altered FC between hippocampal subfields and brain regions involved in spatial orientation and navigation, vestibular and visual processing, as well as emotional regulation. These findings offer novel insights into the pathophysiological mechanisms in BPPV patients with RD following successful CRP.

Erinacines enhance microglial ramification and alleviate Alzheimer's disease pathology in a metabolically stressed model. This study reveals novel mechanisms, including histone deacetylase inhibition, supporting erinacines as a promising therapeutic for Alzheimer's, particularly in cases complicated by metabolic dysfunction.

This study emphasizes the impact of functional segregation-integration preference on the cognitive outcome of cerebral small vessel disease (CSVD). Compared to segregated resting-state network, integrated one was found to contribute to cognitive resilience against mild and moderate damage from CSVD. Cognitive cross-overs exist for several domains before severe damage stages.

Schematic representation of the underlying molecular mechanisms by which ESK mediates neuroprotection of the PI3K/AKT signaling pathway in mice with ICH through activation of NTF3 expression.

Transfer RNA-derived small RNAs (tsRNAs) are generated through the cleavage of transfer RNAs. tsRNAs modulate gene expression through transcriptional and translational mechanisms. tsRNAs are implicated in the pathogenesis of neurodegenerative disorders. tsRNAs have potential applications as nucleic acid therapeutics for the treatment of neurodegenerative diseases.

IL-3 modulates macrophage phagocytic activity and promotes SCI repair. (A) After SCI, IL-3 is secreted by astrocytes surrounding the lesion core, while foamy macrophages filled with lipid droplets gather in the injury center, contributing to the failure of functional recovery in mice. (B) Blockage of IL-3 leads to increased aggregation of macrophage and lipid droplets at the injury core, resulting in the expansion of the lesion area and worsened locomotor function in mice. (C) Administration of IL-3 results in a significant decrease in macrophage accumulation and promotes the clearance of lipid droplets by macrophages at the injury site, accompanied by enhanced functional recovery.

Injection of LPS led to hippocampal CA1 STING overexpression and microglial activation, which upregulated complement C1q-mediated synaptic phagocytosis, resulting in abnormal theta oscillation and decreased LTP, ultimately leading to cognitive impairment.

The study utilized single nucleotide polymorphisms from genome-wide association studies as instrumental variables and employed Mendelian Randomization to uncover causal relationships between epilepsy and both vitamin D and vitamin D-binding protein. Additionally, the findings support that anti-epileptic drugs reduce serum vitamin D levels without affecting vitamin D-binding protein.

This study provided a novel training paradigm, the theta rhythm-based dot probe task, to effectively modify individuals' negative attentional bias. The underlying mechanism of this training may be to facilitate the switch of attention from negative stimuli to positive ones.

All patients underwent a 3-week intervention of combined electromagnetic stimulation. Scale assessments and magnetic resonance imaging data collection were performed before and after the intervention, followed by scale assessments at the eighth week.

An evaluative analysis conducted at our center on PSP patients has uncovered a significant association between alcohol consumption and more pronounced clinical symptoms. Specifically, heavy alcohol consumption exacerbates motor symptoms and accelerate cognitive decline, particularly in visuospatial and executive abilities, memory, and language functions. This correlation is particularly pronounced among male patients.

By integrating brain cell type-specific cis-eQTLs with glioma GWAS dataset using MR and Bayesian colocalization analyses, we elucidated genes with causal effects in distinct brain cell types or glioma subtypes and pinpointed potential brain cell type-specific therapeutic targets.

Patients with SCA3 exhibit asymmetric cerebellar atrophy, particularly more pronounced on the left side, which is associated with motor balance impairments. Additionally, bilateral asymmetric atrophy is observed in the brain, correlating with motor dysfunction.

Seeds-based functional connectivity analysis revealed significant alterations in cognitive networks during microlesion period after deep brain stimulation. Functional connectivity within the three major networks of the default mode network, executive control network, and dorsal attention network showed a widespread decline after surgery.

The JNK-specific inhibitor SP600125 can specifically inhibit the JNK signaling pathway, reduce the expression of the ENT1 transporter, and reduce the seizure intensity in experimental rats. The mechanism is related to the transport of adenosine from the extracellular space to the intracellular space by ENT1 during epileptic states. Inhibition of ENT1 can increase the concentration of adenosine in the extracellular fluid of the hippocampus. The increase in adenosine can inhibit the release of glutamate by acting on the A1 receptor of the presynaptic membrane.

The present study showed the cognitive ability of old-aged rats was decreased than adult and middle-aged rats; males have better cognitive ability than females in middle-aged rats. The neuronal dendritic structures of the hippocampus were damaged to different degrees during aging, and spine loss occurred in females rather than males in middle-aged rats. In addition, the microbial diversity of gut microbiota was significantly decreased in old-aged male rats; some specific bacteria of microbiota communities were changed with aging.

Reduced expression of ANXA1 was observed in the brain cortex of septic mice. ANXA1 deficiency led to a decreased 7-day survival rate and exacerbated neurobehavioral changes induced by CLP. Furthermore, ANXA1 deficiency worsened BBB dysfunction in septic mice, with this effect being mediated through occludin and ZO-1. The protective effects of ANXA1 are mediated by the VEGF-A/VEGF-R2 signaling pathway.

This study explores the relationship between mild traumatic brain injury (mTBI) and disruptions in the default mode network (DMN) using a multimodal approach. Through functional connectivity analysis, diffusion tensor imaging, and gene expression profiling, the research highlights the role of diffuse axonal injury in DMN abnormalities, particularly in the middle cingulate cortex (MCC). The study suggests potential therapeutic targets for neuromodulation, such as the dorsolateral prefrontal cortex (DLPFC), to mitigate cognitive and emotional disturbances associated with mTBI.

TBI leads to the release of exosomes enriched with miR-9-5p, which targets Scd1 in lung tissue, thereby promoting ferroptosis. Treatment with antagomir 9-5p alleviates traumatic brain injury-induced acute lung injury.

This study demonstrated that degeneration of the NBM accompanied by a reduction in the integrity of its WM pathways occurred in MCI patients and was correlated with cognitive impairment. Furthermore, working memory and FC between the NBM and right putamen could be improved by computerized, multidomain, and adaptive cognitive training.

We found structure–function coupling, rather than gray matter volume, spontaneous regional neural activity (ALFF) or uni-modal regional connectivity profile (degree centrality) could predict music perception. Further, structure–function coupling of left middle frontal gyrus (L.MFG), a region that is homologous to typical music circuits, fully mediated the negative link between ALFF of L.MFG and MBEA score.

Exploring the potential targeted therapy of remyelination after spinal cord injury: The review demonstrates the possibility of stimulating oligodendrocyte precursor cell proliferation, differentiation, and myelin sheath formation in both in vitro and in vivo SCI models through molecular pathway modulation and pharmacological agents. Targeted therapies have shown promising results in improving remyelination, providing hope for functional recovery in SCI patients.

Our study indicates that spinal cord stimulation improves consciousness in DOC patients, shown by EEG changes and enhanced P300 metrics. The “ABCD” model and ERP assessments may boost SCS surgery success rates for awakening.