The success of anti-amyloid-β (Aβ) monoclonal antibody has marked the beginning of the disease-modifying therapy (DMT) era for Alzheimer's disease (AD). As these agents are increasingly adopted in clinical practice, the focus of management has gradually shifted from standardized treatment initiation and amyloid-related imaging abnormalities (ARIA) management to long-term management after treatment discontinuation. Based on evidence from recent phase Ⅲ clinical trials, real-world studies, and clinical practice in China, this review summarizes the therapeutic benefits and current limitations of anti-Aβ monoclonal antibody and discusses its clinical value and ongoing challenges in the DMT era.

Dementia with Lewy bodies (DLB) is the second most common type of neurodegenerative dementia after Alzheimer's disease (AD) and represents a major component of the Lewy body disease (LBD) spectrum. In China, the first and second versions of the expert consensus were issued in 2015 and 2021, respectively. With the growing understanding of the clinical features and biomarkers of DLB, and considering recent advances in multidisciplinary diagnostic and therapeutic models as well as clinical practice in China, this updated consensus systematically integrates the latest domestic and international evidence. It provides comprehensive updates on the epidemiology, etiology and pathophysiological mechanisms, clinical manifestations, accessory examinations, diagnosis and differential diagnosis, and treatment strategies of DLB. "Expert recommendation on the diagnosis and management of dementia with Lewy bodies (2026)" emphasizes a diagnostic framework combining core clinical features with indicative biomarkers, as well as the value of multimodal biomarkers in early identification. In addition, it proposes a treatment strategy centered on symptomatic management and multidisciplinary care. The aim is to provide more standardized and practical guidance for clinical diagnosis and treatment, thereby improving the recognition and management of DLB in China.

Microglia, as the resident innate immune cells of the central nervous system, play a pivotal role in both the onset and progression of Alzheimer's disease (AD). Emerging evidence has shown that metabolic reprogramming serves as a critical determinant of microglial functional states and exerts profound effects on AD pathogenesis. In this review, we systematically synthesize recent advances concerning microglial metabolic reprogramming in AD, with particular emphasis on the contributions and underlying mechanisms of glucose, lipid and amino acid metabolism. We further examine how key genetic risk factors including APOE and TREM2 genes drive metabolic perturbations and functional impairment in microglia. The therapeutic promise of targeting metabolic pathways, especially via metabolic modulators such as transient receptor potential vanilloid 1 (TRPV1) agonists, is also underscored. Moreover, we discuss prevailing challenges in the field, including limitations inherent in current disease models and the complexity arising from microglial heterogeneity. Finally, we propose that integrating multi-omics approaches with spatially resolved technologies may enable a more comprehensive dissection of metabolism-immune crosstalk in AD and open new avenues for designing combination therapeutic regimens.

Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is characterized by amyloid β-protein (Aβ) deposition, abnormal tau phosphorylation, synaptic dysfunction, and large-scale network disconnection. With the rapid development of disease-modifying therapy (DMT), neuromodulation targeting neural circuit abnormalities has emerged as an important adjunctive strategy in AD management. Increasing evidence indicates that neuromodulation techniques may exert potential therapeutic effects by reshaping hippocampal-cortical memory networks, modulating neural oscillations, enhancing synaptic plasticity, improving regional brain metabolism, and promoting pathological protein clearance, thereby improving learning memory and overall cognitive function, alleviating clinical symptoms, and potentially delaying disease progression. This review summarizes the mechanisms, clinical evidence, advantages and limitations for invasive techniques [deep brain stimulation (DBS) and vagus nerve stimulation (VNS)] and non-invasive techniques [repetitive transcranial magnetic stimulation (rTMS), transcranial electrical stimulation (TES), transcranial ultrasound stimulation (TUS), gamma entrainment using sensory stimulation (GENUS) and transcranial temporal interference stimulation (tTIS)] in AD.

Objective: To analyze the demographic and regional disparities in the global burden of Alzheimer's disease (AD) from 1990 to 2021, and to predict the evolution trends from 2022 to 2040. Methods: Data were obtained from the Global Burden of Disease 2021 (GBD 2021). We analyzed prevalence, incidence, mortality and disability-adjusted life year (DALY) by age, sex and sociodemographic index (SDI), and projected trends from 2022 to 2040 using Joinpoint regression and Bayesian Meta-regression models. Results: From 1990 to 2021, the global burden of AD showed an overall upward trend. The number of prevalent cases increased from 21.8024 million to 56.8641 million, representing a 160.83% increase, while the age-standardized prevalence rate rose from 672.26 per 100000 to 694.12 per 100000, with an average annual percentage change (AAPC) of 0.10% (95%CI: 0.08%-0.13%). During the same period, the age-standardized incidence rate increased from 117.02 per 100000 to 120.04 per 100000, although trends varied across SDI regions, with a decline observed in high-SDI regions and more pronounced increases in high-middle-SDI regions and middle-SDI regions. In terms of mortality, the number of AD-related deaths increased substantially, whereas the age-standardized mortality remained generally stable, rising from 27.63 per 100000 to 27.91 per 100000 in females and from 20.22 per 100000 to 20.73 per 100000 in males. Regarding DALY, the global age-standardized DALY changed little overall, increasing from 446.26 per 100000 to 451.03 per 100000; in females, it rose from 495.44 per 100000 to 505.32 per 100000, and in males from 363.16 per 100000 to 373.21 per 100000. Conclusions: The global burden of AD was more pronounced among females, older adults and populations in high-middle-SDI regions and middle-SDI regions. Without intervention, AD burden will rise further. Preventive strategies addressing equitable healthcare investment are urgently needed to slow the global rise in AD.

Objective: To compare the differences in clinical characteristics, cognitive function, laboratory and neuroimaging features between patients with dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). Methods: Twenty patients with DLB and 20 patients with PDD diagnosed at The First Hospital of Hebei Medical University from July 2024 to April 2026 were enrolled. Demographic characteristics, time of symptom onset, core clinical symptoms, neuropsychological assessments, including Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), antiparkinsonian medication dosage [levodopa equivalent daily dose (LEDD)], motor function assessed by Unified Parkinson's Disease Rating Scale (UPDRS), as well as neuroimaging and laboratory findings were collected and compared between the 2 groups. Results: Compared with the DLB group, the PDD group had a longer disease duration (Z= -3.279, P=0.001), a longer interval from disease onset to motor symptoms (Z= -3.564, P=0.000), the frequencies of cognitive fluctuations (Fisher's exact probability: P=0.000) and delusions (Fisher's exact probability: P=0.003) were lower. The PDD group showed higher language score (Z= -2.498, P=0.013), lower delayed recall score (Z=2.008, P=0.046), higher total MoCA score (Z= -1.994, P=0.048), and higher visuospatial and executive function score (Z= -3.523, P=0.000). In addition, the PDD group had a higher LEDD (Z= -2.153, P=0.032), lower total bilirubin (Z=1.989, P=0.048) and serum uric acid (Z=2.976, P=0.003), but higher serum sodium (Z= -2.274, P=0.024) and high-density lipoprotein cholesterol (Z= -2.111, P=0.036). Conclusions: Cognitive fluctuation and visuospatial dysfunction are valuable clinical features for differentiating DLB from PDD. Routine biochemical parameters, including serum uric acid, high-density lipoprotein cholesterol and serum sodium, may provide additional clues for the differential diagnosis between these two disorders.

Objective: To investigate the correlation between serum uric acid (SUA) and cognitive function as well as cerebrospinal fluid (CSF) pathological biomarkers in patients with Alzheimer's disease (AD), and to analyze its potential role in the pathophysiological process of AD. Methods: Two independent AD cohorts were recruited from the West China Hospital, Sichuan University between January 2023 and January 2025. The Cohort 1 (cognitive cohort, n=329) included patients with AD confirmed by amyloid β-protein (Aβ)-PET or CSF pathological biomarkers. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Frontal Assessment Battery (FAB), and the association between SUA and cognitive function was evaluated. The Cohort 2 (CSF cohort, n=149) consisted of patients with AD confirmed by CSF pathological biomarkers, in whom CSF levels of Aβ₄₂, Aβ₄₀, phosphorylated tau (p-tau), total tau (t-tau), α-synuclein (α-Syn), and neurofilament light chain (NfL) were measured to investigate the association between SUA and CSF pathological biomarkers. Correlation analysis, multiple linear regression analysis, causal mediation analysis, and interaction analysis were performed to explore the associations among SUA, cognitive function, and CSF pathological biomarkers. Results: In the Cohort 1, correlation analysis showed that SUA was positively correlated with MMSE (r=0.139, P=0.022), MoCA (r=0.198, P=0.001), and FAB (r=0.138, P=0.023) in AD patients. Multiple linear regression analysis showed that SUA was linearly correlated with MoCA in AD patients (standardized partial regression coefficient=0.144, P=0.014). In the Cohort 2, correlation analysis showed that SUA was negatively correlated with CSF Aβ₄₂(r_s= -0.169, P=0.047). Multiple linear regression showed that when FAB was included, SUA was linearly correlated with CSF Aβ₄₂(standardized partial regression coefficient= -0.188, P=0.045). Causal mediation analysis showed that CSF Aβ₄₂did not mediate the associations between SUA and MMSE, MoCA and FAB (P > 0.05, for all), and the effects of SUA on cognitive function were mainly direct effect (MMSE: P=0.004; MoCA: P=0.002; FAB: P=0.000). Interaction analysis showed that CSF Aβ₄₂had significant main effect on MMSE (standardized partial regression coefficient=0.191, P=0.015), MoCA (standardized partial regression coefficient=0.195, P=0.014), and FAB (standardized partial regression coefficient=0.167, P=0.033); SUA had a significant main effect on FAB (standardized partial regression coefficient=0.199, P=0.021); however, the interaction term between SUA and CSF Aβ₄₂was not statistically significant with MMSE, MoCA and FAB (P > 0.05, for all), suggesting that the effect of SUA on cognitive function was not moderated by Aβ₄₂. Conclusions: Higher SUA is associated with better cognitive function in AD patients and with lower CF Aβ₄₂, and no significant mediation or interaction effects were found between two associations.

Objective: To investigate the association between the triglyceride-glucose (TyG) index and cognitive dysfunction in patients with Alzheimer's disease (AD) and comorbid cardiometabolic diseases (CMD). Methods: A total of 265 patients with AD diagnosed at The First Affiliated Hospital of Zhengzhou University from June 2020 to September 2025 were retrospectively enrolled. According to the with or without CMD, patients were divided into the CMD group (n= 137) and the non-CMD group (n= 128). Cognitive function was assessed using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Univariable and multivariable Logistic regression analyses were performed to screen factors for moderate-to-severe dementia in AD patients with comorbid CMD. Results: Compared with the non-CMD group, the CMD group had lower MMSE score (t= -4.542, P=0.001) and MoCA score (t= -4.798, P=0.001). Logistic regression analysis showed that an elevated TyG index was independently risk factors for moderate-to-severe dementia in AD patients with comorbid CMD (OR=3.413, 95%CI: 1.242-9.374; P=0.017). Conclusions: An elevated TyG index was associated with moderate-to-severe dementia in AD patients with comorbid CMD, suggesting that the TyG index may serve as a potential biomarker reflecting cognitive dysfunction severity in this population.

Objective: To translate and culturally adapt the Cohen-Mansfield Agitation Inventory (CMAI), develop a Chinese short version suitable for the cultural context of mainland China (CMAI-cs), and evaluate its reliability and validity among individuals with cognitive impairment attending a memory clinic. Methods: From August 2023 to July 2025, a total of 281 participants aged≥50 years with cognitive impairment and reliable caregivers were enrolled from The First Hospital of China Medical University, constituting the Alzheimer's disease (AD) subgroup (n=80). The scale was translated, back-translated, reviewed by experts, and culturally adapted in accordance with the International Society for Pharmacoeconomics and Outcomes Research (ISPOR) principles for the translation and cultural adaptation of patient-reported outcome measures. Content validity was assessed through expert review. Internal consistency was evaluated using Cronbach's α coefficient, while test-retest reliability and inter-rater reliability were used to assess the stability and consistency of the scale. Validity was examined using the item-level content validity index (I-CVI), exploratory factor analysis, and correlation analysis with the Neuropsychiatric Inventory (NPI) scores. Results: The Cronbach's α coefficient of the CMAI-cs was 0.87, the test-retest reliability was interclass correlation coefficient (ICC)=0.959 (95%CI: 0.929-0.976), and the inter-rater reliability was ICC (2, 2)=0.870 (95%CI: 0.847-0.891). The I-CVI was 0.833-1.000, and the scale-level content validity index based on the average method (S-CVI/Ave) was 0.879. Exploratory factor analysis extracted 5 common factors, with a cumulative variance contribution rate of 66.04%, and the factor loadings of the items on their corresponding factors was 0.61-0.90. Concurrent validity analysis showed that in the overall cognitive impairment cohort, the total CMAI-cs score exhibited an extremely strong positive correlation with the NPI psychiatric behavioral symptom subscore (r_s=0.901, P=0.000) and caregiver distress subscore (r_s=0.887, P=0.000). In the AD subgroup, the total CMAI-cs score also showed an extremely strong positive correlation with the NPI psychiatric behavioral symptom subscore (r_s=0.905, P=0.000) and caregiver distress subscore (r_s=0.895, P=0.000). Conclusions: The CMAI-cs consists of 18 items and demonstrates good reliability and validity among participants with cognitive impairment. It can be used to assess agitation behavior in cognitive impairment populations, particularly in patients with AD, and may provide a localized tool for clinical assessment and future multicenter studies.

Objective: Two cases of autosomal dominant cerebral small vessel disease caused by HTRA1 gene heterozygous mutation were reported. The clinical phenotypes and imaging features of the disease were summarized via literature review. Methods and Results: Two patients with autosomal dominant cerebral small vessel disease caused by HTRA1 gene heterozygous mutation were diagnosed and treated in The Affiliated Hospital of Guizhou Medical University from November 2023 to February 2025. One patient was a 64-year-old male who developed alopecia at the age of 40 and suffered intracerebral hemorrhage at 52 years old. He subsequently experienced recurrent ischemic strokes complicated by cognitive dysfunction and gait abnormalities. MRI showed diffuse white matter hyperintensities, multiple lacunar infarcts and multiple cerebral microbleeds. Genetic sequencing showed a c.404C > A (p.Ala135Asp) heterozygous mutation in the HTRA1 gene. One patient was a 57-year-old female with memory impairment and abnormal gait as initial manifestations. MRI showed multiple white matter hyperintensities and cerebral microbleeds. Genetic sequencing showed a c.905G > A (p.Arg302Gln) heterozygous mutation in the HTRA1 gene, and her son carried the same mutation. The clinical phenotypes of the two patients were heterogeneous, suggesting that gender and age at onset may affect clinical manifestations. Conclusions: Autosomal dominant cerebral small vessel disease caused by HTRA1 gene heterozygous mutation manifests two distinct clinical phenotypes associated with age and gender. Both patients exhibited characteristic diffuse white matter hyperintensities and multiple cerebral microbleeds. The two cases in this study further broaden the clinical phenotypic spectrum of autosomal dominant cerebral small vessel disease caused by HTRA1 gene heterozygous mutation.

Objective: To report a case of symptomatic amyloid-related imaging abnormalities (ARIA) following Lecanemab treatment in patient with mild cognitive impairment due to Alzheimer's disease (AD-MCI), so as to provide references for the clinical safe application of anti β-amyloid (Aβ) monoclonal antibody. Methods and Results: A 63-year-old male patient presented with memory impairment. Mini-Mental State Examination (MMSE) score was 27. MRI showed mild bilateral hippocampal atrophy, and the Aβ-PET Centiloid value was 67.57 CL. Genetic testing identified an APOE ε4/ε4 homozygous genotype. After 4 infusions of Lecanemab, the patient developed severe fatigue, chest distress and decline in activities of daily living. MRI showed symptomatic amyloid-related imaging abnormalities-edema (ARIA-E) and amyloid-related imaging abnormalities-hemorrhage (ARIA-H). Significant resolution of cerebral edema was achieved after anti-inflammatory hormone therapy, yet cerebral microbleeds continued to increase. The MMSE score rose from 27 to 30, and activities of daily living remained stable. Conclusions: Cognitive function improved in the patient with AD-MCI after Lecanemab treatment; nevertheless, symptomatic ARIA-E and ARIA-H may occur as complications. Hormone therapy can alleviate cerebral edema. The APOE ε4/ε4 homozygous genotype represents a high-risk factor for ARIA, and patients often present with atypical symptoms.

Objective: To investigate the predictive value of arterial collateral circulation (ACC), Superficial Venous Drainage Score (SVS) and Deep Venous Drainage Score (DVS) derived from multiphase CTA (mCTA) for 90d neurological function outcome in patients with acute anterior circulation large vessel occlusion (AAC-LVO) ischemic stroke following endovascular treatment (EVT), and to develop predictive models. Methods: Total 148 patients with AAC-LVO ischemic stroke who underwent EVT between April 2020 to March 2025 in Tianjin Huanhu Hospital. All patients underwent mCTA prior to treatment. ACC, SVS and DVS were evaluated based on mCTA. Patients were categorized into good outcome (≤2, n=85) and poor outcome (≥3, n=63) groups based on 90d modified Rankin Scale (mRS) scores. Univariate and multivariate Logistic regression analyses were performed to identify influencing factors for neurological function outcome, based on which prognostic prediction models were established. The predictive efficacy of each model was evaluated using receiver operating characteristic (ROC) curves. Results: Logistic regression analysis showed that poor ACC was an independent risk factor for poor neurological function outcome after EVT in patients with AAC-LVO ischemic stroke (OR=13.601, 95%CI: 1.777-104.105; P=0.012). An high DVS2 score served as an independent protective factor for favorable neurological function outcome (OR=0.019, 95%CI: 0.004-0.094; P=0.000). Three prognostic prediction models were established accordingly. ROC curves showed that area under the curve (AUC) of Model 1 [combining clinical indicators admission National Institutes of Health Stroke Scale (NIHSS) score and ACC] was 0.696 (95%CI: 0.615-0.769, P=0.000). The AUC of Model 2 [combining clinical indicators and venous drainage scores (DVS1, DVS2)] was 0.867 (95%CI: 0.802-0.917, P=0.000). The AUC of Model 3 (combining clinical indicators, ACC and venous drainage scores) was 0.911 (95%CI: 0.854-0.952, P=0.000). Both Model 2 (Z=3.280, P=0.001) and Model 3 (Z=5.731, P=0.000) exhibited significantly better predictive performance for neurological functional prognosis than Model 1, while the predictive efficacy was comparable between Model 2 and Model 3 (Z=1.648, P=0.099). Conclusions: Poor ACC derived from mCTA was a risk factor for poor neurological function outcome after EVT in patients with AAC-LVO ischemic stroke, while a high DVS2 score served as a protective factor for favorable neurological function outcome. The combined model incorporating ACC and venous drainage scores yields favorable predictive performance for long-term neurological function prognosis.

Objective: To investigate efficacy, safety and outcomes of magnetic resonance-guided laser interstitial thermal therapy (MRgLITT) for the treatment of brain metastases. Methods: From January 2022 to August 2024, 98 brain metastases patients underwent robot-assisted MRgLITT at 7 neurosurgical centers across the country were included. The effective rate of ablation was calculated based on tumor volume and ablation range to assess whether effective ablation was achieved; Karnofsky Performance Status (KPS) was used to evaluate functional status at preoperative, one, 3 and 6months after surgery. Kaplan-Meier survival curves were drawn to calculate the survival time. Results: A total of 130 intracranial lesions were found in the 98 patients, with a mean volume of (3.55±3.48)cm³ and the mean ablation volume of (6.65±5.48)cm³. Postoperative assessment showed that 92 patients (93.88%) achieved successful ablation with mean ablation rate was (94.15±10.26)%. The KPS score at one, 3, and 6months after surgery were 86.99±12.49, 85.11±17.09, and 82.24±18.32, respectively. The median overall survival was 15.81 (8.53, 23.82) months, and the one-year survival rate was 63.85%. Total 4 patients (4.08%) experienced postoperative complications. Conclusions: MRgLITT is a safe and effective procedure for treating brain metastases and can provide a new option for the systemic treatment. MRgLITT can achieve a favorable outcome comparable to surgical treatment, and its minimally invasive and safe characteristics make it worthy further application.

Objective: To explore the changes of cerebral blood flow (CBF) in basal ganglia and white matter after ventriculo-peritoneal shunt (VPS) of normal pressure hydrocephalus (NPH) and the relationship with prognosis. Methods: A total of 102 patients with NPH who underwent VPS in Sichuan University Affiliated Chengdu Second People's Hospital from January 2020 to January 2024 were included. Salomon hydrocephalus shunt was used to evaluate the prognosis of VPS at one-year follow-up. Univariate and multiuariate Logistic regression analyses were used to screen the influencing factors of poor prognosis, and based on this, a poor prognosis prediction model was constructed. The area under the curve (AUC), integrated discrimination improvement (IDI) and net reclassification improvement (NRI) of the receiver operating characteristic (ROC) curves of different models were compared, and the Hosmer-Lemeshow goodness of fit test was performed. The relationship between CBF in basal ganglia and white matter and poor prognosis was analyzed by restricted cubic spline and threshold effect analysis. Results: According to the postoperative follow-up, the patients were divided into good prognosis group (n=80) and poor prognosis group (n=22). After operation, CBF in basal ganglia (P=0.001) and white matter (P=0.002) in poor prognosis group was significantly decreased compared with good prognosis group. Analysis results excluding CBF in basal ganglia and white matter showed that age (OR=1.943, 95%CI: 1.535-2.132; P=0.014), course of disease (OR=1.712, 95%CI: 1.465-1.948; P=0.010), diameter of lateral ventricle (OR=1.756, 95%CI: 1.498-2.032; P=0.008), time to get out of bed for the first time (OR=1.689, 95%CI: 1.434-1.845; P=0.017), and length of hospital stay (OR=1.545, 95%CI: 1.356-1.789; P=0.034) were risk factors for poor prognosis, according to which a prediction Model 1 was constructed. The analysis results of CBF in basal ganglia and white matter showed that the risk factors of poor prognosis included age (OR=1.845, 95%CI: 1.516-2.105; P=0.018), course of disease (OR=1.623, 95%CI: 1.432-1.879; P=0.012), diameter of lateral ventricle (OR=1.646, 95%CI: 1.465-2.011; P=0.011), time to get out of bed for the first time (OR=1.543, 95%CI: 1.346-1.764; P=0.025), while CBF in basal ganglia (b=-0.609, OR=0.544, 95%CI: 0.346-0.846; P=0.008) and white matter (b=-0.486, OR=0.615, 95%CI: 0.421-0.894; P=0.006) were protective factors, according to which a prediction Model 2 was constructed. After addition of basal ganglia and white matter, AUC (0.837; 95%CI: 0.862-1.811, P=0.023), IDI (0.080; 95%CI: 0.061-0.116, P=0.000) and NRI (0.749; 95%CI: 0.561-0.887, P=0.000) were significantly increased. Hosmer-Lemeshow showed that Model 2 (χ²=7.254, P=0.875) has better goodness of fit than Model 1 (χ²=6.378, P=0.698). The results of restricted cubic spline showed that postoperative CBF in basal ganglia and white matter were significantly negatively correlated with poor prognosis, especially when the postoperative CBF in basal ganglia was < 44.16ml/(min·100g) and white matter was < 48.69ml/(min·100g). With the decrease of CBF in basal ganglia and white matter after VPS, the risk of poor prognosis in NPH patients increased significantly. Conclusions: After VPS, CBF in basal ganglia and white matter in NPH patients was significantly increased, and its level was negatively correlated with the risk of poor prognosis.

Objective: To identify the risk factors associated of ischemic recurrence in patients with chronic symptomatic severe intracranial vertebrobasilar artery stenosis and to establish a corresponding risk prediction model (Nomogram model). Methods: Total 387 patients with symptomatic severe intracranial vertebrobasilar artery stenosis from January 2017 to March 2025 in Tianjin Huanhu Hospital were retrospectively analyzed and divided into recurrence group (n=97) and non-recurrence group (n=290) according to whether they developed ischemic cerebrovascular events within 90 d of follow-up. Univariate and multivariate Logistic regression analyses were adopted to identify the risk factors of recurrent ischemic cerebrovascular events in patients with chronic symptomatic severe intracranial vertebrobasilar artery stenosis. A Nomogram model was established. Using JavaScript and other network programming languages, we developed the first mobile prediction platform and real-life services for intracranial vertebrobasilar artery stenosis patients to predict their risk of recurrent ischemic cerebrovascular events. Results: Logistic regression analysis showed that high National Institutes of Health Stroke Scale (NIHSS) score at adminssion (OR=1.426, 95%CI: 1.242-1.637; P=0.000), poor collateral compensation (OR=5.786, 95%CI: 3.088-10.482; P=0.000), high low-density lipoprotein cholesterol (LDL-C; OR=1.021, 95%CI: 1.010-1.031, P=0.000), and high fasting blood glucose(FBG; OR=1.015, 95%CI: 1.006-1.025, P=0.002) were risk factors for recurrent ischemic cerebrovascular events in patients with chronic symptomatic severe intracranial vertebrobasilar artery stenosis. The Nomogram model achieved a concordance C-index of 0.805 (95%CI: 0.752-0.854). The Hosmer-Lemeshow goodness-of-fit test demonstrated a favorable fit (P=0.138), with the calibration curve closely aligning with the actual results. A mobile prediction platform was created at https://cossoss.github.io/calc, and this platform demonstrated good predictive ability. Conclusions: High NIHSS score at admission, poor collateral compensation, high LDL-C, and high FBG were the risk factors for recurrent ischemic cerebrovascular events in severe intracranial vertebrobasilar artery stenosis patients. The Nomogram model established based on the identified risk factors had good prediction value, and the created mobile prediction platform further enhances the practical value of the prediction model.

Glioblastoma (GBM) has an extremely poor prognosis, and chimeric antigen receptor T-cell (CAR-T) therapy offers new hope for its treatment. This review systematically discusses the research progress of CAR-T therapy for GBM, analyzing the major challenges related to the blood brain barrier, the immunosuppressive tumor microenvironment, and the high heterogeneity of tumor antigens and antigen escape. It also summarizes opportunities including target innovation and multi-targeting strategies, breakthroughs in local administration routes, and combination therapy approaches, with the aim of providing a reference for optimizing CAR-T therapy strategies and improving patient outcomes in GBM.