Objective Epilepsy-aphasia spectrum (EAS) represents the most common group of childhood epilepsy syndromes, however, the precise source localization of epileptiform discharges remains undetermined. This study aimed to localize and compare the sources of epileptiform discharges across different EAS subtypes using magnetoencephalography (MEG). Methods In this prospective MEG-based study, we recruited 70 patients with EAS, including 52 with self-limited epilepsy with centrotemporal spikes (SeLECTS), 12 with atypical benign partial epilepsy (ABPE), 3 with Landau-Kleffner syndrome (LKS), and 3 with Epileptic Encephalopathy with continuous Spike-and-Waves during sleep (EE-SWAS). Ten independent epileptiform discharges per patient were analyzed using distributed source modeling with standardized low-resolution electromagnetic brain tomography (sLORETA). The spike source density was quantified as current amplitude, and source locations were mapped according to the Desikan-Killiany atlas. Results The source locations of epileptiform discharges differed significantly across EAS subtypes. EE-SWAS exhibited the highest overall current source density, followed by ABPE, whereas SeLECTS and LKS showed the lowest values. Lobar analysis revealed frontal-predominant discharges in EE-SWAS and ABPE, contrasting with temporal-predominant discharges in SeLECTS and LKS. Moreover, patients with secondary generalized tonic‑clonic seizures exhibited higher current source densities than those with only focal seizures, consistent with broader EEG discharge spread. Conclusions This first systematic MEG source analysis across the full EAS reveals a hierarchical gradient from temporo-centric to fronto-centric distribution, paralleling the clinical severity gradient. Our findings highlight the potential of MEG source imaging for phenotyping and pathophysiological stratification in EAS.

Background: Stroke remains a significant cause of persistent long-term disability globally. Post-stroke neuroplasticity is critical for neurological functional recovery and reducing disability. Nevertheless, the existing scoping reviews rarely systematically integrate its intrinsic mechanisms, predictive biomarkers, and actionable intervention strategies. This scoping review aims to map the current research landscape, synthesize the core research findings, and identify existing research gaps in this field. Methods: This scoping review was conducted following the PRISMA-ScR guidelines. Eligible studies published between 31 January 2021, and 31 January 2026, were retrieved from three major mainstream electronic databases: PubMed, Scopus, and Web of Science. All retrieved evidence was synthesized via narrative approach, focusing on core research findings concerning post-stroke neuroplasticity mechanisms, biomarkers, and therapeutic interventions. Results: The existing research on neuroplastic mechanisms following ischemic stroke is predominantly derived from in vitro and animal studies, which have collectively demonstrated multiple core adaptive alterations, including enhanced synaptic plasticity, dendritic and axonal structural remodeling, restored interhemispheric connectivity, endogenous neurogenesis, and functional reorganization of neural networks. In contrast, mechanistic investigations in human stroke patients primarily highlight compensatory activation within peri-infarct tissues and functionally remote brain regions. The relevant clinical biomarkers are mainly imaging and electrophysiological indicators. Research on therapeutic interventions has mainly focused on rehabilitation treatments such as non-pharmacological magnetic stimulation. Conclusions: This scoping review synthesized the current body of evidence on post-ischemic stroke neuroplasticity and identified critical research gaps, particularly regarding multimodal biomarkers and their translational relevance. The present findings confirm that neuroplastic alterations after ischemic stroke are regulated by multiple pathways, among which those involved in synaptic structure, dendrites, and neural network connections exert pivotal effects. Nevertheless, most existing investigations remain confined to in vitro experiments and animal models. The identification of neuroplasticity biomarkers has opened up new avenues for the development of targeted stroke therapies and offers promising prospects for rehabilitative treatment of stroke patients.

Abstract. Background:. Neuroinflammation driven by microglial activation is a key contributor to secondary brain injury after intracerebral hemorrhage (ICH). This study aimed to determine whether transcranial photobiomodulation (tPBM) modulates microglial activation and improves neurological outcomes following ICH. Methods:. In this study, we used a mouse model of ICH induced by collagenase to investigate the effects of tPBM at three different power levels (25, 50, and 100 mW) on neurological function, hematoma volume, brain edema, and blood–brain barrier (BBB) integrity. We conducted neurobehavioral assessments and analyzed the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway through quantitative polymerase chain reaction, Western blotting, and immunohistochemistry. In addition, we used the STING-specific inhibitor H151 and agonist diABZI to elucidate the role of the cGAS-STING pathway in neuroinflammation. Results:. tPBM treatment significantly improved neurological recovery, with optimal effects observed at 50 mW. This treatment reduced hematoma volume, alleviated brain edema, and preserved BBB integrity. Importantly, tPBM inhibited microglial polarization toward a neurotoxic phenotype by suppressing the activation of the cGAS-STING pathway. The use of H151 resulted in decreased neuronal apoptosis and inflammatory cytokine expression, whereas diABZI reinstated inflammatory processes, highlighting the detrimental role of cGAS-STING overactivation in ICH. Conclusions:. tPBM effectively mitigates neuroinflammation and enhances functional recovery after ICH by modulating the cGAS-STING signaling pathway and suppressing neurotoxic microglial activation. This study underscores the potential of tPBM as a novel therapeutic intervention for improving outcomes in patients with ICH, warranting further exploration in clinical settings.

BACKGROUND/AIM:Systemic inflammation influences glioma progression. We evaluated the prognostic value of the white cell-to-lymphocyte ratio (WLR) and aiming to develop a practical survival prediction model. PATIENTS AND METHODS:Patients with glioma from the INSCOC database were retrospectively analyzed and randomly split into training and validation cohorts (7:3). Kaplan-Meier analysis, restricted cubic splines, and Cox regression assessed associations between WLR and overall survival (OS). A WLR-based nomogram was established and internally validated using calibration and decision curve analysis. RESULTS:The optimal WLR cutoff was 4.182. Patients with WLR ≥4.182 had significantly worse OS (p<0.01). Restricted cubic splines showed a positive dose-response relationship between WLR and mortality risk. In multivariable Cox analysis, age, smoking, drinking, and WLR group remained independent predictors of OS (all p<0.05). Sensitivity analyses confirmed robustness. The nomogram showed good discrimination and calibration for predicting 1-, 3-, and 5-year OS and provided greater net clinical benefit than individual clinical factors. CONCLUSION:WLR is an independent, readily available prognostic marker in glioma. A WLR-based nomogram may aid individualized risk stratification and clinical decision-making.

BACKGROUND:Secondary hemophagocytic lymphohistiocytosis (sHLH) with central nervous system (CNS) involvement poses significant diagnostic and therapeutic challenges. This study aimed to characterize the clinical features, laboratory profiles, and prognostic impact of neurological involvement in adult-onset sHLH. METHODS:We analyzed 130 adult sHLH patients, comparing 28 with CNS involvement to 102 without neurological manifestations. Clinical parameters, neuroimaging, cerebrospinal fluid (CSF) profiles, cytokine levels, treatment responses, and survival outcomes were evaluated. RESULTS:Patients with CNS involvement were older (median age, 54 vs. 46 years; p = 0.013) and had higher disease severity (median HScore, 250 vs. 210; p < 0.001). Malignancy-associated sHLH was more prevalent in the CNS-positive group (42.9% vs. 29.4%; p = 0.038). Neurological manifestations included altered mental status, impaired consciousness, and seizures. Neuroimaging revealed abnormalities in 71.4% of the cases, primarily T2-weighted fluid-attenuated inversion recovery hyperintensities and leptomeningeal enhancement. CNS-positive patients exhibited markedly elevated inflammatory markers, most notably CSF Interleukin-6 (p < 0.001). In multivariable analysis adjusted for malignancy, age, ferritin, and HScore, CNS involvement independently predicted mortality (adjusted HR = 2.0, 95% CI: 1.1-3.7, p = 0.023), with a significantly shorter median overall survival (6.5 vs. 11.5 months, p < 0.0001). Malignancy-associated etiology and HScore ≥ 250 were also independent prognostic factors. The DEP (dexamethasone, etoposide, and polyethylene glycol-asparaginase) regimen achieved a faster median time to initial response than the HLH-94 protocol (9 vs. 14 days, p = 0.02). CONCLUSIONS:CNS involvement defines a severe phenotype of adult-onset sHLH, characterized by malignancy-prone etiology, intense neuroinflammation, and poor prognosis. We establish CNS involvement as an independent predictor of mortality, underscoring the critical need for early recognition and CNS-directed therapies.

BACKGROUND:Inflammation is a key mediator for brain injury in acute ischemic stroke (AIS) and the neutrophil-monocyte-to-lymphocyte ratio (NMLR) is a novel composite index for inflammatory. So far, prior studies have not evaluated the prognostic value of NMLR for 3-month functional outcomes in patients with AIS, nor systematically compared its performance with established markers, such as neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and individual cellular components. This prospective cohort study aims to address these research gaps. METHODS:A total of 815 consecutive patients with AIS hospitalized between December 2023 and May 2024 were enrolled. Baseline clinical data and blood samples were collected within 24 h of admission. The primary outcome was poor 90-day functional outcome (modified Rankin Scale score > 2). Multivariable logistic regression determined adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for the outcome association of NMLR. Receiver operating characteristic (ROC) curve analysis compared the predictive performance (area under the curve [AUC]) of NMLR with NLR, MLR, and individual cellular components. RESULTS:Of the 815 patients, 224 (27.5%) had poor functional outcomes. After adjusting for confounders, higher NMLR was independently associated with increased risk of poor outcomes (aOR = 1.370 per unit increase, 95% CI: 1.214-1.546; p < 0.001). NMLR's predictive performance (AUC = 0.708, 95% CI: 0.668-0.749) was statistically equivalent to NLR (AUC = 0.709, p = 0.594), but significantly superior to MLR and individual cellular components (all p < 0.05). CONCLUSIONS:This is the first prospective study to assess the predictive value of the NMLR for 3-month functional outcomes in patients with AIS and systematically compare NMLR with NLR. NMLR can predict poor 90-day outcomes in patients with AIS independently. NMLR is a valid prognostic tool for AIS with performance comparable to NLR.

OBJECTIVE:Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome frequently complicated by severe neurological manifestations, including epilepsy. This study aimed to characterize the clinical phenotype, identify risk factors, and determine outcomes specific to HLH-associated epilepsy. METHODS:We conducted a retrospective cohort study of 76 patients with HLH, comparing those with epilepsy (n = 25) and those without (n = 51). Comprehensive clinical, laboratory, genetic, electroencephalogram, and neuroimaging data were analyzed. RESULTS:Patients with HLH-associated epilepsy were significantly younger and had a higher prevalence of primary HLH. They demonstrated a more severe inflammatory profile, marked by elevated ferritin, interleukin-6, and cerebrospinal fluid (CSF) pleocytosis. Multivariate analysis identified age ≤25 years, ferritin >20,000 ng/mL, CSF pleocytosis, and evolution to cortical atrophy as independent risk factors for epilepsy. Neuroimaging revealed a characteristic "enhancement-to-atrophy" sequence, where acute contrast-enhancing lesions (64.0 % vs. 29.4 %) often progressed to cortical atrophy (56.0 % vs. 19.6 %), highlighting a trajectory from acute neuroinflammation to permanent structural injury. The epilepsy group had significantly poorer survival (median 19 vs. 23 months). Although systemic HLH remission was achieved, the majority of patients (68.0 %) developed refractory epilepsy, necessitating long-term antiseizure medication. SIGNIFICANCE:HLH-associated epilepsy constitutes a severe clinical entity driven by intense neuroinflammation, which frequently results in irreversible brain damage. Early identification of its hallmark features, including young age, extreme hyperferritinemia, CSF pleocytosis, and the distinctive "enhancement-to-atrophy" neuroimaging sequence, is crucial for prompt intervention and long-term neurological management.

Hemorrhage expansion (HE) is associated with morbidity and mortality in acute ischemic stroke hemorrhagic transformation (HT) patients. To address the research gap in HE related to large-artery atherosclerosis acute ischemic stroke with hemorrhagic transformation (LAA-AIS-HT) patients, this study focused on examining the correlation between IBI and HE. We enrolled 357 LAA-AIS-HT patients and categorized into two groups depending on the presence of HE. Information on general demographics, laboratory data, and medical imaging examinations were obtained. The area under the receiver operating characteristic (ROC) curve was used to determine the predictive value. Logistic regression analysis was performed to assess comparison. A total of 357 LAA-AIS-HT patients enrolled in the study, 258 patients (72.3

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-beta (A(3) and leading to cellular senescence and cognitive deficits. Cellular senescence contributes significantly to the pathogenesis of AD through the senescence-associated secretory phenotype (SASP), exacerbating A(3 deposition. This study investigates the protective effects of 3-N-Butylphthalide (NBP), a compound derived from Apium graveolens Linn (Chinese celery), on A(3-induced cellular senescence in U87 cells. Using RNA-sequencing and biochemical assays, we demonstrate that NBP ameliorate A(3 oligomer-induced cellular senescence and apoptosis, and regulated the expression of cyclin-dependent kinase inhibitor 2A (CDKN2A) and components of the cyclin-dependent kinase 2 (CDK2)- phosphorylated retinoblastoma 1 (pRB1)-Caspase3 pathway. Moreover, NBP was shown to suppress the expression of SASP-related genes. These findings suggest that NBP rescues U87 cells from A(3 oligomer-induced senescence and apoptosis through modulating the CDK2-pRB1-Caspase3 axis and SASP expression. Our results underscore the potential of NBP as a senostatic agent for AD which have not been reported in previous studies, offering insights into its mechanisms of action and paving the way for future studies on its efficacy in vivo and in clinical settings. Thus, we contribute to growing evidence supporting the use of senolytic and senostatic agents in the treatment of AD.

This paper aimed to probe the role of the LINC00641/miR-323a-3p/EIF4G2 axis in regulating behavioral and brain monoamine neurotransmitter levels in a mouse model of depression induced by chronic unpredictable mild stress (CUMS). A CUMS-induced depression model was established in mice. A series of behavioral tests, comprising the sucrose preference, tail suspension, as well as forced swimming tests, were conducted. Levels of LINC00641, miR-323a-3p, and EIF4G2 in hippocampal tissues were measured. Biochemical indices, including 5-HT, NE, and DA, were analyzed. Hippocampal neuron structure and apoptosis were evaluated. The targeting relationship among LINC00641, miR-323a-3p, and EIF4G2 was validated experimentally. CUMS mice exhibited reduced sucrose preference, prolonged immobilization time in behavioral tests, decreased 5-HT, NE, and DA levels, and increased hippocampal neuron apoptosis. Overexpression of LINC00641 or knockdown of miR-323a-3p significantly alleviated depression-like behaviors and restored monoamine neurotransmitter levels. LINC00641 regulated EIF4G2 expression by targeting miR-323a-3p, while miR-323a-3p and EIF4G2 also modulated depression through LINC00641. Upregulation of LINC00641 improves depression-like behaviors and enhances monoamine neurotransmission in CUMS mice via the miR-323a-3p/EIF4G2 axis, underscoring its potent as a therapeutic target for depression.

OBJECTIVE:To explore the effects of knowledge-attitude-practice (KAP) nursing and guided intervention on mental state, sleep quality, and self-efficacy of cancer patients. METHODS:Retrospectively, 106 cancer patients were collected and divided into the control (received routine nursing and psychological intervention) and observation groups (given KAP nursing combined guided intervention) following different nursing modalities. The psychological status of patients was evaluated by the Self-rating Anxiety Scale (SAS) and Self-rating Depression Scale (SDS). Disease uncertainty in patients was assessed by Mishel Uncertainty in Illness Scale (MUIS). The quality of life of patients was evaluated by using the short form 36 health survey questionnaire. Sleep quality was evaluated by the Pittsburgh Sleep Quality Index (PSQI). The knowledge level, coping ability, self-efficacy, and satisfaction with nursing work were observed. RESULTS:Following nursing intervention, the scores decreased, with the observation group exhibiting lower scores in SAS, SDS, MUIS, and PSQI. The observation group demonstrated higher levels of cognitive functioning, self-efficacy, and nursing satisfaction and superior coping abilities. The quality of life of both groups after nursing was improved, with the observation group showing a higher score. CONCLUSION:Guided intervention and KAP nursing can improve the mental status, sleep quality, and self-efficacy of cancer patients.

Essential tremor (ET) is a highly prevalent movement disorder characterized by high heritability. However, the genetic basis of this disease remains largely unknown. Understanding the genetic causes of ET is crucial for unravelling its pathogenesis and developing targeted therapies. In this study, we aimed to investigate tandem repeats in a Chinese cohort of ET pedigrees. To explore the genetic causes of ET, we enrolled 165 Chinese ET pedigrees and performed whole-exome sequencing as well as long-read sequencing within this cohort. Quantitative real-time PCR and western blot analyses were employed to assess HSF1 expression levels. Transgenic Drosophila model and induced pluripotent stem cells (iPSCs) were constructed to investigate the pathogenic role of HSF1 in ET. Our study identified the expanded variable number of tandem repeats (VNTRs) in intron 10 of HSF1. Long-read sequencing revealed two repeat configurations consisting of CCCCGCNCCGCCT and CCNCGCCT in these VNTR loci. Expanded VNTR alleles were highly enriched in ET-affected individuals, and the length of VNTRs was positively correlated with disease severity. We found the intronic repeat expansions downregulated HSF1 expression in affected individuals, indicating its loss-of-function in ET. Consistently, RNAi knockdown of HSF1 homolog in Drosophila led to leg and head shaking and age-dependent movement deficits, recapitulating the ET phenotype in the fly model. iPSCs derived from the ET-affected individual carrying expanded VNTRs in the HSF1 gene exhibited significantly reduced expression of HSF1 compared to control iPSCs. Bulk RNA-sequencing analysis of these iPSCs revealed that diminished HSF1 expression resulted in the downregulation of genes associated with GABAergic synapse function. In conclusion, our study suggests that impaired GABAergic signalling may play a critical role in the pathogenesis of HSF1-related ET. These findings provide new information on the aetiology of ET and highlight the role of HSF1 in human genetic disorders.

BackgroundThis study evaluated the long-term safety, tolerability and effectiveness of rimegepant, 75 mg orally disintegrating tablet, for the acute treatment of migraine in Chinese adults.MethodsThis phase 3, multicenter, open-label, single-arm study enrolled Chinese adults with a ≥1 year history of migraine (with or without aura), 6-18 moderate-to-severe migraine attacks/month within three months before a screening visit and at least six migraine days during a 30-day observation phase (OP). After the OP, eligible participants took rimegepant as needed (maximum one tablet per day) at the onset of mild-to-severe migraine attack for a long-term treatment (LTT) of 52 weeks.ResultsOverall, 240 participants were treated and 208 (86.3%) completed the study. During LTT, 203 (84.6%) participants reported ≥1 treatment-emergent adverse event (TEAE) and 46 (19.2%) reported ≥1 TEAE considered to be rimegepant-related. There were no rimegepant-related serious AEs or rimegepant-related TEAEs that led to treatment interruption or discontinuation. Mean reduction from the OP in monthly migraine days was observed as early as the first four weeks (-1.7; 95% confidence interval = -2.2 to -1.2), with an overall mean reduction of -4.4 (95% confidence interval = -4.9 to -3.9) days across LTT.ConclusionsRimegepant had a favorable long-term safety profile, was well tolerated in Chinese participants, and a reduction in the number of monthly migraine days was observed during the LLT.Trial registration: ClinicalTrials.gov identifier: NCT05371652.

There is no approved effective drug for diabetic peripheral neuropathic pain (DPNP) in China. Gabapentinoids including mirogabalin have shown promise, although data in Chinese patients are scarce. This phase 3, multicenter, randomized, double-blind, placebo-controlled trial investigated the efficacy and safety of mirogabalin for treating DPNP in China. Mirogabalin was administered at 5 mg twice daily for the first week and uptitrated to 15 mg twice daily for a total duration of 14 weeks. The primary efficacy endpoint was the change from baseline in weekly average daily pain score (ADPS) at week 14; secondary endpoints included the ADPS responder rate, Short-Form McGill Pain Questionnaire visual analogue scale score, patient global impression of change (PGIC), average daily sleep interference score (ADSIS), EuroQol 5-dimensions 5-levels (EQ-5D-5L), and incidence of treatment-emergent adverse events (TEAEs). Of 393 patients (mirogabalin, n = 196; placebo n = 197), the mean age was 58.2 years (mirogabalin, 58.7 years; placebo, 57.7 years) and 54.2

AbstractBackgroundWe aimed to investigate the relationship between systemic immune‐inflammation index (SII) and short‐term mortality in acute ischemic stroke (AIS) with internal carotid artery (ICA) severe stenosis and stroke associated pneumonia (SAP) patients.MethodsInformation on general demographic, laboratory data, CT angiography, magnetic resonance angiography, or digital subtraction angiography were obtained. The predictive power was evaluated by assessing the area under the receiver operating characteristic (ROC) curve. The logistic regression was performed to assess the association of SII and short‐term mortality in severe stenosis ICA‐AIS and SAP patients.ResultAmong 342 patients with severe stenosis ICA‐AIS and SAP, death occurred in 66 patients during 120 days follow‐up. Multivariate regression analyses indicated that increased SII predicts higher mortality in 120 days follow‐up, and the risk of short‐term mortality in SII > 666.31 × 109/L group is increased 4.671‐fold. Patients with SII > 666.31 × 109/L had higher proportion of male, hypertension, smoking, higher admission NIHSS score, higher systolic blood pressure, and higher proportion of 120 days mortality. Higher SII predicted a worse 120 days mortality was worked out by Kaplan–Meier methods.ConclusionAn elevated SII was remarkably associated with 120 days mortality in severe stenosis ICA‐AIS and SAP patients.

Previous studies have found the effect of ShuganJieyu capsule and St. John’s wort on the treatment of depression and explored their potential benefits for somatic symptoms, while the evidence of comparison of them for depression with somatic complaints is lacking. In this multicenter randomized controlled trial, 198 major depressive disorder (MDD) patients with somatic complaints were randomly allocated, 92 in the ShuganJieyu capsule group, and 91 in the St. John’s wort group completed 8 weeks treatment. Primary outcome was the change score of the 17-item Hamilton Depression Rating Scale (HDRS-17) at week 8. Secondary outcomes included other indices of depression, somatic symptoms, anxiety, insomnia, quality of life, and adverse events. The change scores of HDRS-17 were not significantly difference between the two groups, but the reduction in HDRS-17 was significantly improved in both the ShuganJieyu capsule (HDRS-17Δ = − 11.35 ± 5.38, p < 0.001) and St. John’s wort (HDRS-17Δ = − 11.20 ± 5.71, p < 0.001) groups. The other outcomes showed similar results. Compared with St. John’s wort, the ShuganJieyu capsule induced significantly greater HDRS-17 reductions in male (SMD, − 0.55; 95% CI, − 1.08 to − 0.02) but not in female. Overall, The ShuganJieyu capsule was comparable to St. John’s wort as a complementary and alternative intervention for MDD patients with somatic complaints in the acute treatment, especially for male patients.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) and leading to cellular senescence and cognitive deficits. Cellular senescence contributes significantly to the pathogenesis of AD through the senescence-associated secretory phenotype (SASP), exacerbating Aβ deposition. This study investigates the protective effects of 3-N-Butylphthalide (NBP), a compound derived from Apium graveolens Linn (Chinese celery), on Aβ-induced cellular senescence in U87 cells. Using RNA-sequencing and biochemical assays, we demonstrate that NBP ameliorate Aβ oligomer-induced cellular senescence and apoptosis, and regulated the expression of cyclin-dependent kinase inhibitor 2A (CDKN2A) and components of the cyclin-dependent kinase 2 (CDK2)- phosphorylated retinoblastoma 1 (pRB1)-Caspase3 pathway. Moreover, NBP was shown to suppress the expression of SASP-related genes. These findings suggest that NBP rescues U87 cells from Aβ oligomer-induced senescence and apoptosis through modulating the CDK2-pRB1-Caspase3 axis and SASP expression. Our results underscore the potential of NBP as a senostatic agent for AD which have not been reported in previous studies, offering insights into its mechanisms of action and paving the way for future studies on its efficacy in vivo and in clinical settings. Thus, we contribute to growing evidence supporting the use of senolytic and senostatic agents in the treatment of AD.

Background:Acute coronary syndrome (ACS) presents with a variable prognosis, posing significant public health challenges. This study investigated the potential link between cerebral small vessel disease (CSVD) burden and outcomes in patients with ACS. Methods:In this retrospective cohort study, ACS patients admitted to Beijing Friendship Hospital, Capital Medical University, Beijing, China from January 2020 to October 2021, were analyzed. CSVD burden was assessed using magnetic resonance imaging markers, including white matter lesions, lacunar infarcts, cerebral microbleeds, and enlarged perivascular spaces. The correlation between CSVD burden and clinical outcomes, including major adverse cardiovascular and cerebrovascular events, myocardial infarction (MI), target vessel revascularization, stroke, and mortality was examined over a one-year follow-up. Results:Out of 248 patients, 216 patients were categorized into the low score group (LSG-CSVD) and 32 patients were categorized into the high score group (HSG-CSVD). Patients in the HSG-CSVD group exhibited significantly worse prognosis, with an elevated risk of major adverse cardiovascular and cerebrovascular events, MI, and target vessel revascularization. After adjusting for age, sex, hypertension, troponin T, and estimated glomerular filtration rate, a significantly higher risk of MI was observed in the HSG-CSVD group (HR = 4.51, 95% CI: 1.53-13.26, P = 0.006). Subgroup analysis by age and sex consistently demonstrated increased adverse outcomes in the HSG-CSVD. Conclusions:The study highlights a direct association between increased CSVD burden and poorer ACS outcomes, particularly in MI risk. These findings underscore the importance of considering CSVD burden as a crucial prognostic factor in ACS management, facilitating risk stratification and guiding personalized treatment strategies.

Transcranial photobiomodulation refers to irradiation of the brain through the skull using low-intensity red or near-infrared light, which is the most commonly studied method of light energy biotherapy for central nervous system disorders. The absorption of photons by specific chromophores within the cell elevates ATP synthesis, reduces oxidative stress damage, alleviates inflammation or mediates the activation of transcription factors and signaling mediators through secondary mediators, which in turn trigger downstream signaling pathways to cause a series of photobiological effects including upregulation of neurotrophic factors. Multiple mechanisms are simultaneously involved in the pathological process of central nervous system disorders. The pleiotropic treatment of transcranial photobiomodulation towards multiple targets plays a beneficial role in improving hemodynamics, neural repair and improving behaviors in central nervous system disorders such as ischemic stroke, traumatic brain injury, neurodegenerative diseases, epilepsy and depression. This review mainly introduces the mechanism and recent preclinical and clinical advances of transcranial photobiomodulation for central nervous system disorders, which will provide a reference for clinicians to understand and engage in related studies, and calls for more and larger studies to validate and develop a wider application of transcranial photobiomodulation in central nervous system.

Postoperative stroke is a challenging and potentially devastating complication after elective carotid endarterectomy (CEA). We previously demonstrated that transmembrane protein 166 (TMEM166) levels were directly related to neuronal damage after cerebral ischemia-reperfusion injury in rats. In this subsequent clinical study, we aimed to evaluate the prognostic value of TMEM166 in patients suffering from post-CEA strokes. Thirty-five patients undergoing uncomplicated elective CEA and 8 patients who suffered ischemic strokes after CEA were recruited. We evaluated the protein level and expression of TMEM166 in patients diagnosed with postoperative strokes and compared it to those in patients who underwent uncomplicated elective CEA. Blood samples and carotid artery plaques were collected and analyzed. High expressions of TMEM166 were detected by immunofluorescence staining and Western Blot in carotid artery plaques of all patients who underwent CEA. Furthermore, circulating TMEM166 concentrations were statistically higher in post-CEA stroke patients than in patients allocated to the control group. Mean plasma concentrations of inflammatory markers, including interleukin 6 (IL-6) and C-reactive protein (CRP), were also elevated in patients with postoperative strokes. Therefore, based on these findings, we hypothesize that elevated TMEM166 levels, accompanied by a strong inflammatory response, serve as a useful biomarker for risk assessment of postoperative stroke following CEA.