Anti-N-methyl-d-aspartate-receptor (NMDAR) encephalitis often leads to long-term cognitive impairments, including deficits in executive function, even after acute symptoms resolution, but the underlying mechanisms remain unclear. To explore this, a murine model was established via 14-day intracerebroventricular (ICV) infusion of anti-GluN1 IgG. Mice exhibited deficits in cognitive flexibility and short-term recognition memory, as evidenced by impaired performance in reversal learning and in the novel object recognition test, while spatial learning and anxiety-related behaviors were spared. Molecular analyses revealed decreased expression of GluN1 and GABAergic markers (GAD67, vGat) in the medial prefrontal cortex (mPFC). This disinhibition likely underlies the increased recruitment of excitatory neurons in the mPFC as suggested by the c-Fos expression, which may contribute to the cognitive rigidity in anti-GluN1 IgG-infused mice. Moreover, ex vivo electrophysiological recordings from mPFC pyramidal neurons showed increased sensitivity of spike generation together with diminished inhibitory synaptic input in anti-GluN1 IgG-infused mice. Together, these findings point to mPFC dysfunction, possibly involving GABAergic disruption and local disinhibition, as a candidate mechanism contributing to persistent cognitive rigidity in NMDAR antibody-associated encephalitis.

BACKGROUND:Chronic nonspecific low back pain (CNLBP) is a prevalent global health issue. Previous studies have demonstrated comorbidity between hyperalgesia and mood disorders in nerve growth factor (NGF)-induced CNLBP rat models. The Wnt/β-catenin signalling pathway plays a pivotal role in chronic pain pathogenesis by modulating glial cell activation and synaptic plasticity. However, the mechanism of this pathway underlying CNLBP and related emotional disorders remains unclear. METHODS:Mechanical and thermal hypersensitivity were measured via Von Frey and hot/cold plate tests, while anxiety-like and depression-like behaviours were evaluated through the elevated plus maze (EPM), open field (OFT), and forced swim tests (FST). Additionally, electrophysiology, immunofluorescence, and western blot were employed to investigate the underlying mechanisms in CNLBP model rats. Furthermore, the effects of intrathecal IWR-1 (a Wnt/β-catenin signalling pathway inhibitor) on CNLBP rats were examined. RESULTS:The Wnt/β-catenin signalling pathway was activated in NGF-CNLBP model rats. Three consecutive days of intrathecal IWR-1 administration significantly alleviated mechanical hyperalgesia (≥ 10 days), cold hyperalgesia (≥ 9 days), and heat hyperalgesia (≥ 4 days), while improving anxiety-like behaviours in CNLBP rats. IWR-1 reduced ACC pyramidal neuron excitability and excitatory transmission and suppressed glial activation in the spinal dorsal horn in CNLBP rats. Notably, IWR-1 selectively downregulated spinal NR1 (N-methyl-D-aspartate receptor subunit 1) protein expression level in CNLBP rats. CONCLUSIONS:Inhibiting spinal Wnt/β-catenin signal pathway attenuates CNLBP-related hyperalgesia and anxiety and modulates ACC neuronal excitability, glial activity, and NR1 expression. SIGNIFICANCE STATEMENT:Modulating the spinal Wnt/β-catenin signalling pathway may be pivotal for elucidating the mechanisms underlying hyperalgesia and anxiety-like behaviour in chronic nonspecific low back pain (CNLBP).

Background:Parkinson's disease (PD) is a multifactorial neurodegenerative disease with a high prevalence worldwide, leading to motor and non-motor symptoms. Moreover, PD presents a progressive aggravation alongside time, the middle and late patients in PD requires the use of a variety of anti-Parkinson's drugs with obvious side effects, which bring serious impact on the quality of life of patients. In recent years, repetitive transcranial magnetic stimulation (rTMS), as a kind of non-invasive neuromodulation therapy, has drawn increasing interest from neurologists, and has been effectively utilized to alleviate both motor and non-motor symptoms of PD. However, the treatment protocols and therapeutic effects of rTMS for PD patients are inconsistent. This meta-analysis aims to systematically evaluate the safety and efficacy of rTMS therapy in patients with PD. Methods:We will perform a comprehensive search in the following electronic databases: PubMed/Medline, Web of Science, EMBASE, and Cochrane, without language restrictions, from their inception to September 2024. This review protocol was formulated according to the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P) guidelines. The Cochrane risk of bias tool is utilized to assess the risk of bias. Finally, the effect size was expressed by a standardized mean difference (SMD) with a 95% confidence interval (CI). Results:A total of 45 randomized controlled trials were included. The results of enrolled studies indicated that both primary and secondary indicators had improved. Subgroup analysis showed that high-frequency rTMS (HF-rTMS) targeting the supplementary motor area (SMD =  - 0.56; 95 %CI = [-0.77, -0.36]; p < 0.00001), primary motor cortex (SMD: -1.65; 95 %CI = [-2.35, -0.95]; p < 0.00001), and dorsolateral prefrontal cortex (DLPFC) (SMD: -0.68; 95 %CI = [-1.16, -0.21]; p = 0.005) yielded a significant reduction in motor UPDRS-III scores, compared to the sham group. In addition, HF-rTMS over left DLPFC or intermittent theta burst stimulation over left DLPFC may benefit cognition. Furtherly, the subgroup analysis of the Beck Depression Inventory scores indicated HF-rTMS over the left DLPFC was a beneficial treatment for depressive symptoms in PD. Conclusion:The meta-analysis showed that rTMS was effective and safe in the treatment of PD, improving motor function (such as a decrease in UPDRS-III total scores, subscores of UPDRS-III, and FOG-Q scores) in patients with PD and leading to improvement in cognitive function and depression (such as an increase in MocA scores and a decrease BDI scores). Although the results of the subgroup analysis provide a valuable reference for the selection of rTMS for clinical application, further larger multicenter, randomized, placebo-controlled studies with a large number of participants are still required to validate these results.

Cognitive impairment involves sustained deficits across several key domains: memory, executive function, attention, and behavioral regulation. The condition encompasses cognitive dysfunction linked to Alzheimer's disease, mild cognitive impairment, vascular cognitive impairment, and other forms of neurodegeneration. Existing pharmacotherapies frequently yield inconsistent clinical benefits, are often accompanied by side effects, and generally lack disease-modifying properties. These limitations have spurred increasing attention toward safe, repeatable non-pharmacological strategies. Non-invasive brain stimulation, a central non-pharmacological tool, can regulate excitability in targeted brain regions, shape network-level connectivity, and facilitate activity-dependent neuroplasticity. Evidence from multiple clinical settings supports its potential to improve cognitive outcomes. This review centers on major NIBS techniques: repetitive transcranial magnetic stimulation, transcranial electrical stimulation, gamma-frequency sensory stimulation, photobiomodulation, and transcranial ultrasound stimulation. We synthesize their underlying mechanisms, clinical applications, and supporting evidence, aiming to provide an evidence-based framework to guide standardized clinical implementation and future research design in this area.

Since its inception in 2017, temporal interference stimulation (TIS) has attracted increasing attention as a novel neuromodulation approach with the potential to non-invasively target deep brain structures. As the field moves from initial biophysical validation toward broader experimental and translational applications, a macroscopic understanding of its developmental trajectory and thematic evolution is needed. In this study, we systematically mapped the scientific landscape of TIS research using bibliometric methods to characterize its knowledge structure, core themes, and emerging frontiers. The analysis shows that TIS research has expanded rapidly from foundational animal studies and biophysical mechanism validation toward computational head modeling, individualized electric field optimization, and early human applications. Current research is increasingly focused on cross-species scaling, stimulation dosimetry, comparative advantages over other neuromodulation techniques, precise targeting strategies, and potential physiological risks such as high-frequency conduction block. Overall, TIS is evolving from an exploratory biophysical concept into a promising but technically and physiologically complex neuromodulation tool. Overcoming current engineering and translational barriers, particularly through individualized modeling, rigorous optimization, and well-designed human studies, will be essential for establishing TIS as a reliable therapeutic intervention.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by coordinated dysfunction across multiple brain cell types. Natural compounds with multi-target regulatory potential represent promising therapeutic candidates, yet their cell-type-specific mechanisms in the human AD brain remain incompletely understood. In this study, we integrated ligand-based target prediction with large-scale single-nucleus RNA sequencing (snRNA-seq) data from 201,074 nuclei obtained from AD and control human brain samples, together with subcluster-level functional profiling, cell-cell communication analysis, transcriptional regulatory network inference, and structure-based molecular docking and molecular dynamics simulations to systematically characterize the multicellular actions of isofraxidin. Our analyses identified 19 high-confidence isofraxidin targets exhibiting distinct enrichment patterns across AD-associated cell populations. Key targets-including ALOX5 in microglia, MAOB in astrocytes, HSPA1A in endothelial cells (EC), and CBR1 in oligodendrocytes (ODC)-were preferentially localized to disease-relevant cellular subclusters. snRNA-seq revealed marked remodeling of these cell types in AD, characterized by inflammatory microglia, reactive astrocytes, stress-impaired ECs and neurodegeneration-associated ODCs, which overlapped with the highest target enrichment. Functional and regulatory analyses indicated that these vulnerable states converge on oxidative stress, metabolic dysregulation, proteostasis impairment, and aberrant inflammatory signaling. Molecular docking and 100-ns molecular dynamics simulations further confirmed stable and energetically favorable binding of isofraxidin to its core targets. Collectively, this integrative single-cell framework delineates the cell-type-specific therapeutic landscape of isofraxidin in AD and highlights its potential to coordinately modulate key pathogenic pathways underlying neurodegeneration.

BACKGROUND:As common manifestations of depression, somatic symptoms are associated with treatment-resistant depression and a poor prognosis. Existing therapy for somatic symptoms, such as antidepressants and psychotherapy, have limited efficacy. Therefore, seeking effective and acceptable therapy for somatic symptoms is vital. OBJECTIVE:This study aimed to evaluate the efficacy and safety of transcranial direct current stimulation (tDCS) over the dorsomedial prefrontal cortex (dmPFC) in depressed patients with somatic symptoms. METHODS:The tDCS over the dmPFC was administrated to depressive patients for 2 weeks using a randomized, double-blind, sham-controlled design. Clinical symptoms were assessed at baseline, following tDCS, and 6 weeks after the treatment session. Structural neuroimaging data were collected to build individualized finite element models. Computed median and maximum current density values in the dmPFC and bilateral amygdala regions of interest (ROIs) were correlated with the alleviated somatic symptoms. RESULTS:Sixty-five patients were initially in the study; 57 completed the trial. The active group displayed greater improvements in somatic symptoms compared to the sham group after tDCS. During follow-up, the active group showed a higher responder ratio than the sham group, though not a greater improvement. Furthermore, there was a positive correlation between individualized electric fields of the right amygdala and changes in somatic symptoms in the active group. CONCLUSION:The tDCS targeting dmPFC was shown to be an effective and acceptable complementary therapy for depressed patients with somatic symptoms. The right amygdala electric field was associated with alleviation of somatic symptoms following tDCS treatment.

Lesion network mapping (LNM) has emerged as a popular framework to map the network mechanism of brain disorders using lesions and normative brain connectome (NBC) 1 . It was first demonstrated in neurological symptoms and was rapidly extended to a broad range of brain disorders in the past decade. A recent study by Van den Heuvel et al. questioned the methodological foundations of LNM 2 . We here raise concerns regarding their errors and biases in the methodology and visualization. The conclusion of that study—LNM maps circumscribed brain changes mostly to one and the same outcome—is not supported by the data presented.

INTRODUCTION:Cerebral Small Vessel Disease (CSVD) is one of the most common causes of vascular cognitive impairment and dementia, and there is still a lack of effective treatment options. High-Definition Transcranial Direct Current Stimulation (HD-tDCS) is a non-invasive neural regulation method with promising prospects in the treatment of cognitive impairment. Therefore, we explore whether HD-tDCS can improve cognitive function and potential mechanisms in patients with CSVD. METHODS:This study was divided into two complementary parts. Part 1 involved 104 patients with CSVD and 36 matched Healthy Controls (HCs) to establish the optimal HD-tDCS stimulation target. Part 2 enrolled an additional 20 patients with CSVD who received a 2-week HD-tDCS intervention targeting the stimulation site identified in Part 1. Cognitive assessments and multimodal magnetic resonance imaging data were collected from all participants at both baseline and follow-up. RESULTS:In part 1 of the study, the patients with CSVD showed significant differences in Montreal Cognitive Assessment (MoCA), Auditory Verbal Learning Test (AVLT)-study, AVLT-immediate, AVLT-delay, AVLT-recognition, Trail Making Test (TMT)-A, TMT-B, and Verbal Fluency Test -fruits/vegetables compared with HCs. Meanwhile, left hippocampal subregions to whole-brain resting state-functional connectivity (rs-FC) analysis showed that the rs-FC strength between the hippocampal cognitive subregion (HIPc) and both the left dorsolateral superior frontal gyrus and the right medial superior frontal gyrus significantly altered in patients with CSVD compared with HCs, suggesting that the prefrontal cortex is a stimulation target of HD-tDCS. In part 2 of the study, performance on the MoCA, AVLT-study, AVLT-delay, SDMT, and digit span test improved in 20 patients with CSVD after 14 days of HD-tDCS targeting the left dorsolateral prefrontal cortex. At the same time, the rs-FC strength between HIPc and the alteration cluster found in the first part of the study, located in the left dorsolateral superior frontal gyrus, was decreased after treatment. DISCUSSION:HD-tDCS may help normalize brain network function and improve cognitive function in patients with CSVD by reducing rs-FC between the hippocampus and the left dorsolateral prefrontal cortex. Further research is needed to refine treatment plans and evaluate the long-term effects of HD-tDCS on cognitive function in patients with CSVD. CONCLUSION:The patients with CSVD exhibited altered rs-FC in the hippocampal-prefrontal circuit. HD-tDCS could modulate this circuit and improve cognitive function in patients with CSVD.

While many polygenic risk scores (PRSs) of coronary artery disease (CAD) have been developed to stratify disease risks in Europeans, their performances in the Chinese population are suboptimal due to population heterogeneity. Considering the complex genetic architecture of CAD, we train a multi-ancestry multi-trait PRS for CAD, termed PRSCAD+, which is optimized in a prospective Chinese cohort to integrate information from large-scale genome-wide association studies (GWASs) of CAD and 15 related traits in East Asians and Europeans. The hazard ratio (HR) for incident CAD is 1.26 (95% confidence interval: 1.21-1.31) per standard deviation of PRSCAD+, which is stronger than published PRSs, East Asian-specific multi-trait PRS, and the single-trait PRS of CAD. PRSCAD+ also increases the concordance index (C-index) by an average of 1.1% over 14 published PRSs (ΔC ranges from 0.4% to 1.6%; P < 0.05). Addition of PRSCAD+ to traditional clinical risk factors led to a significant improvement in the C-index by 1.3% (P < 0.05). In an external validation set (mean age 58 years), PRSCAD+ achieved an odds ratio of 2.40 (2.18-2.65) and an area under the receiver operating characteristic curve of 0.799 (0.782-0.816) for predicting early-onset CAD. Furthermore, we observed significant gradients across the quintiles of PRSCAD+ in both datasets. These results demonstrate that PRSCAD+ can improve risk prediction and stratification of CAD in the Chinese population by incorporating genetic information of related traits from both European and East Asian studies.

BACKGROUND:Resilience is increasingly conceptualized as a dynamic process rather than a static trait. The Mount Sinai Resilience Scale (MSRS) captures this process by assessing the frequency and subjective efficacy of malleable resources employed to manage stress. This study aimed to validate the Chinese MSRS (C-MSRS) and investigate the psychometric and network features of resilience in healthy and clinical populations. METHODS:The MSRS was translated and administered to 600 healthy adults and 95 patients. We utilized Exploratory and Confirmatory Factor Analyses, reliability and validity assessments, network analysis, and quadrant analysis to evaluate the psychometric properties and characterize clinical resilience profiles. RESULTS:The C-MSRS demonstrated satisfactory psychometric properties, yielding a 21-item, five-factor model. Network analysis identified the "Meaning and Purpose" dimension (specifically hope and growth mindset) as the central hub, functioning as a "motivational engine" that integrates other resilience resources. Clinical profiling revealed distinct phenotypes: depression was characterized by global deficits consistent with amotivation and helplessness (low frequency/low efficacy), whereas anxiety patients exhibited preserved motivational drive in social connections. Furthermore, "Meaning and Purpose" emerged as a core transdiagnostic factor negatively correlated with symptom severity. CONCLUSIONS:The C-MSRS is a robust, process-oriented instrument for the Chinese context. Our findings highlight resilience as an active, cognition-motivated process organized around hope and growth mindset. By capturing distinct resilience deficits in depression versus anxiety, the C-MSRS offers a precise tool for dissecting resilience mechanisms and guiding targeted interventions.

Background Social anxiety disorder (SAD) is associated with dysfunctions in face processing, a critical aspect of social interaction. However, there is a dearth of biomarkers that could facilitate precise diagnosis and targeted treatment. Aims This meta‐analysis seeks to investigate abnormalities in P1, N170, LPP, and N2pc during face processing in individuals with SAD. It also aims to examine the role of potential moderators. Methods A systematic review of the literature yielded 32 relevant studies, encompassing the aforementioned ERP components: P1 (21 studies), N170 (16 studies), LPP (11 studies), and N2pc (6 studies). We performed a random‐effects meta‐analysis to calculate Hedges′ g and assessed publication bias using the trim‐and‐fill method. Risk of bias was evaluated across five domains using an adapted Downs and Black checklist. Results Risk of bias was generally low, with some concerns regarding external validity. Primary analysis showed enhanced P1 ( g = 0.92) and LPP ( g = 1.07) amplitudes in SAD. However, the P1 effect became nonsignificant ( g = 0.20) after adjusting for publication bias, whereas the LPP enhancement remained robust. No significant differences were found for N170 or N2pc. Mixed‐model analysis indicated that P1 and N2pc exhibited the largest absolute effect sizes. No significant moderators (age, clinical status and task type) were identified. Conclusions The findings highlight the LPP as the most robust neural correlate of face processing deficits in SAD, reflecting impaired late‐stage attentional disengagement. Although P1 amplitudes appear enhanced, this effect is likely inflated by publication bias. Current evidence does not support consistent alterations in N170 or N2pc. LPP may serve as a promising potential biomarker for the clinical diagnosis and treatment monitoring of SAD.

Background The molecular mechanisms linking brain function alterations to gene expression in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis remain unclear. Methods We analyzed the coefficient of variation of blood oxygenation level dependent signal (CVBOLD) and functional connectivity (FC) in 30 healthy controls and 42 patients, with classification via 5 machine learning models. Transcriptomic profiles from the Allen Human Brain Atlas and neurotransmitter density maps from positron emission tomography were integrated. Partial least squares (PLS) regression determined gene expression relevant to the CVBOLD/FC changes. Multivariate linear regression evaluated neurotransmitter contributions. Results Anti-NMDAR encephalitis patients exhibited increased CVBOLD in the right superior parietal gyrus, right fusiform gyrus, right lingual gyrus, left fusiform gyrus and left paracentral lobule meanwhile disrupted FC mainly in default mode and salience networks. PLS analysis revealed 2,320 genes significantly associated with CVBOLD/FC (pbonferrni < 0.05), enriched in synaptic signaling (MAPK, cAMP), metabolic regulation (insulin resistance), and neurodegeneration pathways. Hub genes PPARGC1A (positive correlation with CVBOLD/FC) and UBA52 (negative correlation) were validated in key brain regions. Neurotransmitter analysis showed norepinephrine (NAT) strongly contributed to CVBOLD (weight = 0.57, pFDR < 0.001), meanwhile serotonin (5HT4), cannabinoid (CB1), noradrenaline (NAT), and glutamate (NMDA) influenced FC. Conclusion This study identifies a transcriptional signature that is spatially associated with CVBOLD/FC abnormalities and neurotransmitter distributions in anti-NMDAR encephalitis, thereby generating hypotheses about molecular targets that may be relevant for future mechanistic studies and precision medicine.

Apathy is a highly prevalent and disabling neuropsychiatric syndrome, but its multi-dimensional structure is a challenge for progress towards better identification and treatment. A crucial unresolved question is whether social disengagement reflects a distinct deficit in social motivation or a by-product of diminished initiative or emotional blunting. Previous studies have been constrained by modest sample sizes and limited use of apathy-specific instruments or phenotypically narrow cohorts. Here, we analysed item-level data from 11,243 individuals recruited across multiple centres, including 1154 neurological patients with Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, autoimmune encephalitis and small vessel disease, alongside people with depression and healthy adults. Across exploratory and confirmatory factor analyses, symptom-level network modelling, and lifespan analyses, social apathy consistently emerged as a coherent and separable dimension. This pattern was preserved across health, psychiatric, and neurocognitive cohorts, from adolescence through late life. Recognising social apathy as an independent domain reframes a central aspect of mental health—the motivation to connect, care, and act for others—and provides a foundation for more precise assessment and for interventions targeting both social and neurobiological mechanisms.

Parkinson's disease (PD) is an incurable neurological disorder that often begins insidiously with sleep disturbances and somatic symptoms, progressing to whole-body motor and cognitive symptoms1-5. Dysfunction of the somato-cognitive action network (SCAN)-which is thought to control action execution6,7 by coordinating arousal, organ physiology and whole-body motor plans with behavioural motivation-is a potential contributor to the diverse clinical manifestations of PD. To investigate the role of the SCAN in PD pathophysiology and treatments (medications, deep-brain stimulation (DBS), transcranial magnetic stimulation (TMS) and MRI-guided focused ultrasound stimulation (MRgFUS)), we built a large (n = 863), multimodal, multi-intervention clinical imaging dataset. Resting-state functional connectivity revealed that the substantia nigra and all PD DBS targets (subthalamic nucleus, globus pallidus and ventral intermediate thalamus) are selectively connected to the SCAN rather than to effector-specific motor regions. Importantly, PD was characterized by specific hyperconnectivity between the SCAN and the subcortex. We therefore followed six PD cohorts undergoing DBS, TMS, MRgFUS and levodopa therapy using precision resting-state functional connectivity and electrocorticography recording. Efficacious treatments reduced SCAN-to-subcortex hyperconnectivity. Targeting the SCAN instead of effector regions doubled the efficacy of TMS treatments. Focused ultrasound treatment benefits increased when the target was closer to the thalamic SCAN sweet spot. Thus, SCAN hyperconnectivity is central to PD pathophysiology and its alleviation is a hallmark of successful neuromodulation. Targeting functionally defined subcortical SCAN nodes may improve existing therapies (DBS, MRgFUS), whereas cortical SCAN targets offer effective non-invasive or minimally invasive neuromodulation for PD.

Emerging studies have consistently shown that blood-oxygenation-level-dependent signals within white matter (WM) appear to be related to neural activity. This recognition of WM functional signal has provided a great opportunity to investigate how the brain’s WM functionally evolves in youth as well as its relationship to developmental disorders. Using multimodal imaging data from 407 participants aged 8 to 22 years, we constructed the WM functional connectome (WMFC) as well as the WM structural connectome (WMSC). Our findings reveal a global three-stage reorganization process in WMFC characterized by a decreasing-increasing-decreasing pattern. Regional changes are marked by hierarchical development between primary networks and higher-order networks. In conjunction with the WMSC, we measured WM SC‒FC coupling, and found that coupling monotonically decreases with development. Treating these spatial patterns as phenotypes of WM function, we demonstrated significant regulation by neurotransmitter receptors and transcriptomic expression. Notably, WMFC significantly explained the heterogeneous regional vulnerability in neurodevelopmental disorders and outperformed the WMSC in predicting cognitive function. This study underscores the importance of investigating WM function in understanding the neural mechanisms of brain maturation and disorders.

Background: Intracranial atherosclerotic stenosis (ICAS) is a significant risk factor for cognitive impairment, likely via hypoperfusion. Despite the growing number of studies on ICAS, the efficacy of endovascular treatment (EVT) in improving the cognitive function of ICAS patients remains uncertain. This study aims to explore (1) whether EVT can improve the cognitive function of ICAS patients, (2) the correlation between cerebral perfusion and cognitive impairment. Methods: We conducted a prospective cohort study (NCT06336174) of non-acute anterior circulation ICAS patients, assigned to EVT plus best medical treatment (EVT group) or best medical treatment alone (BMT group). Cognitive function was assessed using a battery of neuropsychological tests, and cerebral blood flow (CBF) was quantified using pseudo-continuous arterial spin labeling at baseline and 3-month follow-up. The efficacy of EVT on cognitive function was evaluated using linear mixed-effects models (LMM). Pearson correlation analysis was used to assess the correlation between cognitive changes and perfusion changes. Multivariate linear regression (MLR) was used to identify the predictors of cognitive improvement (Figure 1). Results: 106 participants completed the follow-up, with the BMT group (n = 62, 42 males, age 55.62 ± 9.79, education 6.97 ± 3.76), and the EVT group (n = 44, 35 males, age 57.95 ± 8.20, education 6.42 ± 2.74). LMM analysis showed significant group × time interactions in immediate verbal memory (Auditory Verbal Learning Test, AVLT-immediate, F = 6.777, p = 0.011), working memory (Digit Span Test backward, F = 8.036, p = 0.005), and frontal lobe fluency (Verbal Fluency Test, semantic-VFT, F = 8.345, p = 0.005), which were primarily driven by significant improvements in the EVT group, as well as inter-group differences at follow-up (Figure 2). The EVT group showed significant improvement in CBF at follow-up, and this was correlated with better semantic-VFT performance (r = 0.568, p = 0.017) (Figure 3). MLR analysis showed that EVT improved neuropsychological scores, with greater effects in those with lower baseline scores. Conclusions: Endovascular treatment significantly improved cognitive function in non-acute ICAS patients, associated with the improvement in CBF, particularly in those with worse baseline cognitive performance. Further studies with larger sample sizes and longer follow-up are needed to confirm the long-term benefits and to explore the underlying mechanisms.

BackgroundNeglect dyslexia (ND) is an acquired reading disorder that is associated with unilateral spatial neglect (USN), typically resulting from right hemisphere damage. While the majority of related research has focused on alphabetic written languages, identifying omission and substitution errors linked to specific cognitive mechanisms, it remains unclear whether similar error patterns appear in Chinese ND, given the unique structural characteristics of the Chinese reading system.AimThis study aimed to determine (1) whether phonetic component position in pictophonetic characters modulates error types, (2) how lexicality and word length influence errors in compound words, and (3) how first versus last characters contribute to omission and substitution errors in Chinese ND.Methods and ProceduresSixteen right-hemisphere stroke patients with left USN completed a tailored reading battery comprising pictophonetic characters (left/right phonetic components), two-/three-character real words and pseudowords, and three-character real word pairs with first- or last-character substitutions. Omission and substitution error rates were quantified. Analyses included mixed-effects models, and Fisher's exact tests.Outcomes and ResultsThe position of the phonetic component in pictophonetic characters influenced omission errors but had no effect on substitution errors. In compound words, omission errors increased with word length and for pseudowords, reflecting attentional and lexical demands. Substitution errors showed a strong lexicality effect (near-absent in real words) but no word length effect, indicating a pre-lexical origin. The first character was critical for error patterns.Conclusions and ImplicationsThe findings reveal a double dissociation between error types in Chinese ND. Substitution errors appear to be driven by visual crowding, while omission errors are affected by structural and lexical factors. This supports error-based subtyping and tailored interventions: perceptual training for substitution errors, and spatially-guided attention training for omission errors.