睡眠剥夺是导致神经炎症、氧化应激及认知功能障碍的重要诱因，其机制与星形胶质细胞的活化密 切相关。星形胶质细胞作为中枢神经系统的关键调控者，通过A1/A2极化表型在睡眠剥夺中发挥双重作 用：A1型通过释放促炎因子和神经毒素加剧神经炎症及突触损伤，而A2型则通过分泌神经营养因子和抗 炎介质促进神经修复。本文系统综述了睡眠剥夺中星形胶质细胞的活化机制及相关信号通路：NF-κB通 路、MAPK通路在、SHH通路和JAK-STAT通路。研究表明，慢性睡眠剥夺通过炎症介质积累及星形胶质 细胞过度激活导致认知障碍，而调控其极化表型（如抑制A1型或增强A2型）可能成为干预睡眠剥夺相关 神经损伤的新策略。未来需进一步解析星形胶质细胞极化的时空特异性及信号网络交互作用，为靶向治 疗提供理论依据。

To systematically evaluate the impact of virtual reality (VR) technology on cognitive function in stroke patients. Methods: A computer-based search was conducted across multiple domestic and international databases for randomized controlled trials (RCTs) investigating VR interventions in patients with post-stroke cognitive impairment. The search period spanned from the inception of the databases to January 7, 2025. The Cochrane Collaboration's Risk of Bias tool and the Physiotherapy Evidence Database (PEDro) scale were employed to assess the quality of the included studies. Data analysis was performed using RevMan 5.4.1 software. Results: A total of 14 studies, involving 723 patients, were ultimately included. All included studies were of high quality, with PEDro scale scores ranging from 6 to 10. Meta-analysis results indicated that VR technology significantly improved the Montreal Cognitive Assessment (MoCA) score [MD=2.53, 95% CI (0.82, 4.24), P=0.004], the Mini-Mental State Examination (MMSE) score [MD=1.68, 95% CI (1.12, 2.24), P<0.00001], the P300 latency [MD=－25.48, 95% CI (－38.99, －11.96), P=0.0002], the P300 amplitude [MD=0.72, 95% CI (0.14, 1.30), P=0.02], and the Barthel Index or Modified Barthel Index (BI or MBI) score [MD=5.14, 95% CI (3.25, 7.03), P<0.00001] in stroke patients with cognitive impairment. However, no significant effects were observed on the Trail Making Test Part A (TMT-A) score [MD=－12.47, 95% CI (－27.16, 2.23), P=0.10] or the TMT-B score [MD=－ 44.35, 95% CI (－ 117.45, 28.74), P=0.23]. Conclusion: VR technology can improve cognitive function and activities of daily living (ADL) abilities in stroke patients.

To conduct a visual analysis of relevant literature on the application of artificial intelligence in Parkinson's disease research through bibliometric analysis. Methods: The Web Of Science core database was used as the data source for this paper. CiteSpace 6.3.R1 and VOSviewer1.6.20 software were used to conduct bibliometric analyses on the annual number of publications, country/region, institution, keywords, authors and cited literature. Results: Ultimately, 2 043 articles meeting the criteria were included, and the number of publications in this field has been growing rapidly. Articles in this research area have been published by a total of 87 countries/regions. Among them, the United States, China, and Italy are high-yield countries, with Harvard Medical School being the leading institution. The top three authors in terms of publication volume are Gabriella Olmo, Alice Nieuwboer, and Lynn Rochester. High-frequency keywords in this field mainly include Parkinson's disease, deep brain stimulation, and gait, etc.; the latest emerging term is rehabilitation. The application of AI in the field of Parkinson's disease (PD) is mainly distributed in neuroscience, electrical engineering, clinical neurology, and other fields. Among the journals where papers are published, SENSORS ranks first in both publication volume and H-index, while MOVEMENT DISORDERS has the highest impact factor (IF). The most frequently co-cited literature primarily focuses on the integration of electroencephalogram (EEG) signals with AI technology for the early diagnosis of PD. Conclusion: In recent years, AI has been developing rapidly in the medical field, and its application to PD has been increasing year by year, mainly focusing on the prediction of risk factors, diagnosis and treatment of PD.

Traditional intervention methods for fear-related psychological disorders (such as specific phobia and post-traumatic stress disorder) are challenged by drug dependence and insufficient cultural adaptability. Music therapy, with its non-invasive nature and cross-cultural potential, has emerged as a new option, but there is still a gap in the integration of its mechanisms and the fusion of traditional Chinese and Western medical theories. Through a systematic review of recent studies, this paper proposes an integrated model of“Five Elements Music - Neural Plasticity”, which for the first time links the frequency characteristics of the Chinese Yu mode music (40~80 Hz) with the regulation of neurotransmitters (5-HT, GABA) and the functions of the limbic system (amygdala, hippocampus). This paper further constructs a ternary model of“frequency - neurotransmitter – emotion”, providing evidence-based guidance for the setting of music parameters, and proposes the neural mechanism by which group intervention alleviates social anxiety through the mirror neuron system. This paper provides theoretical basis and practical guidance for the standardized treatment of fear-related psychological disorders with music therapy.

Cuproptosis is a newly discovered form of cell death in recent years, while Alzheimer's Disease (AD) is a progressively developing neurodegenerative disorder of the central nervous system with insidious onset. Copper is involved in multiple pathogenic mechanisms of AD, and copper imbalance can induce the death of neurons and glial cells through these distinct mechanisms, thereby contributing to the onset of AD. This review summarizes recent research on the involvement of cuproptosis in the pathogenesis of AD.

Spasticity is a movement disorder caused by the high excitability of the stretch reflex, which is characterized by the speed-dependent enhancement of the tonic stretch reflex with tendon hyperreflexia. It is a common complication in patients with upper motor neuron injury. Surgical treatment is an effective treatment for patients with severe spasticity who fail to respond to drug and physical therapy. In order to ensure the smooth operation and good effect, the patient should be professionally evaluated before operation. This article summarizes the application and prospect of peripheral nerve surgery and emerging neuromodulation techniques in the field of spasm treatment. These techniques aim to improve the spasticity of patients and promote brain plasticity by reducing muscle tension and re-establishing the connection between the injured site and the brain, which is of great significance to improve the quality of life of patients.

Chronic fatigue syndrome (CFS) is closely related to the imbalance of mitochondrial homeostasis, and studies have shown that mitochondria in CFS patients or model animals have abnormalities in morphology and structure, metabolism and quality control, which are closely related to the occurrence and/or development of CFS. In this paper, we take mitochondrial homeostasis as an entry point to systematically sort out its influence and role in the pathogenesis of CFS, with a view to providing more ideas and strategies for the study of potential mechanisms and treatment of chronic fatigue syndrome.

The gut-muscle-brain axis, acting as a three-dimensional interactive network that mediates neurodegenerative diseases and sarcopenia, plays a core regulatory role in the pathological progression of Parkinson’s disease (PD). This article provides a systematic review of how gut microbiota dysbiosis within this axis influences the balance of muscle protein synthesis and degradation via microbial metabolites, how myokines secreted by skeletal muscle in turn modulate neuroinflammation and the function and integrity of the intestinal barrier, and the molecular mechanisms underlying the bidirectional propagation of α-synuclein among the gut, muscle, and brain. Incorporating the latest clinical evidence, it further explores targeted intervention strategies such as probiotics and combined exercise-nutrition approaches, aiming to offer new perspectives for the precision prevention and management of sarcopenia in elderly PD patients.

The potential impact of light pollution on the nervous system is attracting increasing attention and has become a new research field in neuroscience. This review systematically explores the complex interaction mechanisms between light pollution and photosensitive epilepsy (PSE). Evidence indicates that light pollution, especially blue light exposure at 480 nm, significantly elevates seizure susceptibility through two principal pathways: primarily through direct suppression of melatonin secretion via intrinsically photosensitive retinal ganglion cells (ipRGCs) and secondary disruption of circadian rhythms. Core mechanisms involve three pathological dimensions: abnormal elevation of neuronal excitability, dysregulation of circadian clock gene expression patterns, and exacerbation of epileptogenic processes through oxidative stress and neuroinflammatory pathways. Current intervention strategies encompass chronotherapeutic approaches, melatonin supplementation protocols, and public health policy initiatives. Future research should focus on interdisciplinary integration and the application of new technologies to develop personalized precision prevention and treatment strategies, providing a scientific basis for mitigating the potential harm of light pollution on the nervous system.

Progressive non-fluent aphasia (PNFA) is a neurodegenerative disease, a clinical subtype of primary progressive aphasia, characterized by gradually slowing, intermittent language expression and increasing grammatical errors. Current studies have shown that PNFA is mainly associated with abnormalities in tau protein and TAR DNA binding protein-43 (TDP-43), and may involve multiple protein pathologies. In terms of diagnosis, researchers have used imaging techniques such as magnetic resonance imaging (MRI), positron emission tomography (PET), and radiomics to discover specific brain structural changes in patients with PNFA, providing a basis for early diagnosis. In terms of treatment, speech and language therapy and non-invasive brain stimulation techniques (such as transcranial direct current stimulation and transcranial magnetic stimulation) have shown certain improvement effects, but the progress of pharmacotherapy is currently limited.

To investigate the effects of Tafa2 on microglial functional phenotypes, neuronal injury, and functional recovery following acute cerebral ischemia. Methods: Transient middle cerebral artery occlusion (tMCAO) models were established in adult male wild-type mice. The spatiotemporal expression pattern of Tafa2 protein after cerebral ischemia was determined using immunofluorescence techniques. tMCAO models were established in adult male wild-type and Tafa2-knockout mice. The effects of Tafa2 deletion on microglial polarization, neuronal apoptosis, and neurological function during the acute phase of cerebral ischemia were assessed using immunofluorescence, Nissl staining, TUNEL staining, and behavioral tests. Results: In wild-type mice, Tafa2 protein expression was significantly increased in the ischemic hemisphere on day 3 after tMCAO compared to that in the sham group. On day 3 after tMCAO, Tafa2-knockout mice exhibited reduced infarct volume, decreased neuronal apoptosis, and alleviated sensorimotor deficits compared to wild-type mice. 3 days after tMCAO, Tafa2-knockout mice showed an increased proportion of CD206 + microglia and enhanced phagocytic function compared to wild-type mice. Conclusion: Tafa2 deficiency promotes the polarization of microglia toward an anti-inflammatory and pro-repair phenotype, reduces neuronal damage and improves neurological function during the acute phase of ischemic stroke.

showed partial recovery compared to the inducer group but still exhibited abnormalities. On postoperative day

MicroRNAs are tiny RNAs widely expressed in eukaryotic organisms, exhibiting differential expression in numerous diseases. MicroRNA-122 (miR-122) is a signaling molecule closely associated with neurological diseases and has been extensively studied in cerebrovascular diseases. This article provides a review of the role and mechanisms of miR-122 in cerebrovascular diseases, aiming to offer new research targets for cerebrovascular diseases and a theoretical basis for the development of related drugs.

To explore the clinical characteristics, differential diagnosis, surgical outcomes, and prognosis of primary intraspinal melanoma and pigmented neurilemmoma. Methods: A retrospective analysis was conducted on the clinical data of 5 patients with primary intraspinal melanoma and 7 patients with primary intraspinal pigmented neurilemmoma, all of whom underwent surgical treatment and were pathologically confirmed. The clinical characteristics, key points of differential diagnosis, surgical outcomes, and prognosis of these two diseases were analyzed. Results: The 12 patients exhibited non-specific clinical characteristics, primarily presenting with symptoms of spinal cord impairment at the corresponding lesion levels. On conventional MRI, both the 5 cases of primary intraspinal melanoma and the 7 cases of primary intraspinal pigmented neurilemmoma generally showed isointense or hyperintense signals on T1WI and isointense or hypointense signals on T2WI at the corresponding levels. There were certain differences in MRI contrast-enhanced imaging: primary intraspinal melanoma typically demonstrated heterogeneous enhancement with ill-defined borders and invasion of adjacent tissues, while primary intraspinal pigmented neurilemmoma mostly showed homogeneous enhancement with relatively well-defined borders. For the 5 cases of primary intraspinal melanoma, the surgical duration ranged from 80 to 212 minutes, with an average of (140 ± 46) minutes; intraoperative blood loss ranged from 100 to 600 mL, with an average of (260±100) mL; and there were no perioperative deaths. Postoperative MRI revealed complete resection in 2 cases, subtotal resection in 2 cases, and partial resection in 1 case. For the 7 cases of primary intraspinal pigmented neurilemmoma, the surgical duration ranged from 100 to 228 minutes, with an average of (150±48) minutes; intraoperative blood loss ranged from 120 to 580 mL, with an average of (250±80) mL; and there were no perioperative deaths. Postoperative MRI showed complete resection in all 7 cases. Among the 5 patients with primary intraspinal melanoma who were regularly followed up after surgery, 4 patients died within 3 to 15 months after discharge, with a median survival time of 8.5 months. The cause of death in all cases was distant metastasis. One patient had a survival time exceeding 24 months and showed no signs of local recurrence or metastasis as of the last follow-up (June 2024). All patients completed at least 6 months of follow-up. The 7 patients with primary intraspinal pigmented neurilemmoma underwent regular postoperative imaging monitoring. All patients were followed up for 12 to 60 months, and all were alive with no evidence of tumor recurrence or metastasis. Conclusion: Primary intraspinal melanoma and pigmented neurilemmoma exhibit non-specific clinical characteristics. MRI can be used for preliminary differential diagnosis, but pathological results are required for definitive identification. Primary intraspinal melanoma is more severe than pigmented neurilemmoma. Microscopic total tumor resection is the preferred treatment option, and postoperative adjuvant radiotherapy and chemotherapy can prolong patient survival. Pigmented neurilemmoma is mostly a benign tumor, and total tumor resection can generally be achieved. Postoperative radiotherapy and chemotherapy are usually not required, but long-term prognosis is difficult to predict.

Central nervous system (CNS) disorders, characterized by dysfunction and pathology in neurovascular units, represent a leading cause of disability, with high incidence and protracted courses. Tissue inhibitors of metalloproteinase 1 (TIMP-1) serve as natural inhibitors of matrix metalloproteinase 9 (MMP-9) and are critical for maintaining extracellular matrix homeostasis. Recent research has unveiled novel, MMP-independent functions of TIMP-1, as it acts as a multifaceted cell factor by binding to cell surface receptors. Fluctuations in TIMP-1 levels directly correlate with the occurrence and prognosis of CNS diseases, making TIMP-1 a promising target for promoting neurovascular unit repair. This review summarizes the recent research progress of TIMP-1 in CNS diseases, aiming to comprehensively explore its roles and mechanisms in the development of cerebrovascular injury, epilepsy, and neurodegenerative diseases.

Multimodal MRI can describe structure, function and perfusion changes of epilepsy from different perspectives, offering advantages such as multi-sequence, multi-plane imaging, high resolution, and non-invasiveness. This paper elaborates on the current application status, challenges faced, and future development directions of multimodal MRI technology in the field of clinical evaluation of epilepsy. It summarizes its role in locating the epileptogenic zone and improving diagnostic accuracy, analyzes the current limitations and corresponding countermeasures, and looks forward to the prospects of integrating this technology with other techniques.

and protein expression levels of NLRP3, GSDMD, and their downstream inflammatory factors were significantly

To explore rehabilitation options for dysphagia induced by Coronavirus disease 2019 (COVID-19) in post-stroke patients. Methods: A patient with post-stroke sequelae who developed COVID-19-induced dysphagia for more than one month underwent a two-stage comprehensive assessment and treatment. In the first stage, intermittent theta burst stimulation (iTBS) to the bilateral swallowing cortex, balloon dilation therapy, and standard swallowing rehabilitation exercise were performed five times per week for two weeks. In the second stage, iTBS was applied to the suprahyoid muscles for an additional two weeks. Assessments were performed before treatment (T0), after the first stage (T1) and after the second stage (T2). The assessment indicators included the Standardized Swallowing Assessment (SSA), Yale Pharyngeal Residue Severity Rating Scale (YPR-SRS) and Penetration-Aspiration Scale (PAS) based on Flexible Endoscopic Evaluation of Swallowing (FEES), Functional Oral Intake Scale (FOIS), Motor Evoked Potentials (MEP) of suprahyoid muscles, and Functional Near-Infrared Spectroscopy (fNIRS). Results: Compared with T0, there was no significant improvement in swallowing function at the end of T1, with moderate to severe residue observed in the epiglottic vallecula and pyriform sinus. The patient could only attempt minimal liquid intake. Compared with the end of T1, the patient's swallowing function was significantly improved at the end of T2, with the SSA score decreasing from 32 to 22. YPR-SRS improved from moderate/severe residue to mild/trace residue, the PAS score decreased from 4 to 1, and the FOIS increased from 2 to 6. The patient could consume food orally with the exception of large gulps. The MEP latency reduced, and the amplitude increased in the bilateral suprahyoid muscles. The fNIRS results revealed a significant increase in the functional connectivity of the cortical swallowing network. Conclusion: iTBS to the suprahyoid muscles and bilateral swallowing cortex combined with balloon dilation is a safe and effective rehabilitation therapy for treating post-COVID-19 dysphagia in post-stroke patients, potentially by improving the function of the supraglottic muscles and increasing the excitability of swallowing-associated cortical areas and functional connectivity of brain networks.

Mirror Visual Feedback Therapy is an emerging rehabilitation approach derived from the mirror neuron theory, which has been increasingly applied in the rehabilitation of post-stroke motor aphasia in recent years. Mirror visual feedback therapy can effectively ameliorate speech disorders in patients with post-stroke motor aphasia, enhancing their spontaneous speech, repetition, naming abilities, and articulation clarity, thereby improving their capacity for daily communication. This paper discusses the background and development of mirror visual feedback therapy, the therapeutic apparatus involved, its potential mechanisms of action in the treatment of post-stroke motor aphasia, and its clinical applications, aiming to provide novel insights for the rehabilitation of post-stroke motor aphasia.

To analyze the potential latent classes of rehabilitation self-efficacy in elderly patients during the rehabilitation phase after stroke and its relationship with self-care ability. Methods: A total of 44 elderly patients in the rehabilitation phase after stroke were selected. During their rehabilitation treatment, they were surveyed using a general information questionnaire, the Stroke Rehabilitation Self-Efficacy Scale, the National Institutes of Health Stroke Scale, the Self-Rating Anxiety Scale, the Self-Rating Depression Scale, the Modified Barthel Index, and the Mini-Mental State Examination. Mplus 8.3 software was employed to conduct latent profile analysis of patients' rehabilitation self-efficacy. SPSS 26.0 software was used to compare the self-care ability of patients with different rehabilitation self-efficacy classes. Results: The rehabilitation self-efficacy of elderly patients in the rehabilitation phase after stroke was divided into two potential latent classes: the average rehabilitation self-efficacy type (27.78% ) and the good rehabilitation self-efficacy type (72.22%). Age, educational level, stroke type, primary caregiver, compliance with rehabilitation exercises, degree of neurological impairment, anxiety, depression, cognitive dysfunction, and dysphagia were predictive factors influencing the latent profile classes of rehabilitation self-efficacy in these patients. There were differences in the self-care ability classification between the two potential latent classes of rehabilitation self-efficacy (P<0.01). Conclusion: The rehabilitation self-efficacy of elderly patients in the rehabilitation phase after stroke can be classified into two types, and there are differences in self-care ability among patients with different rehabilitation self-efficacy classes.

To explore the possible subtypes and clinical characteristics of persistent postural-perceptual dizziness(PPPD). Methods: A total of 106 patients diagnosed with PPPD were selected from the Shanxi People’s Hospital between May 2023 and December 2023. General and clinical data of the patients were collected; upon admission, questionnaires including the Niigata PPPD Questionnaire(NPQ), Dizziness Handicap Inventory(DHI), Hospital Anxiety and Depression Scale(HADS), and State-Trait Anxiety Inventory(STAI) were administered. Factor analysis was conducted on the scale items, followed by cluster analysis based on the results of the factor analysis, with characteristic analysis performed for each patient group. Results: Factor analysis revealed three factors, named active motor factor(32.82% ), visual stimulation factor(14.80% ), and upright position factor(10.97% ). Cluster analysis identified three subtypes: visual stimulation-dominant subtype(n=25), posture control-dominant subtype(n=24), and active motor-dominant subtype(n=57). There were statistically significant differences in age, occupation, and family history of headaches among the three subtypes(P<0.05). The visual stimulation-dominant subtype patients had younger ages, with a notable family history of headache, and worked primarily as bank/supermarket clerks; the posture control-dominant subtype mainly consisted of civil servants, teachers; while the active motor-dominant subtype included predominantly workers, farmers. No statistically significant differences were found in other clinical data(P>0.05). Conclusion: The most common exacerbating factor for PPPD is active movement; it can be divided into three subtypes, each with significant characteristics in terms of age, occupation, and family history of headaches.

To explore the research status, hot spots and trend of abnormal gait in children with spastic cerebral palsy (SCP). Methods: With Web of Science core collection as the data source, CiteSpace 6.1. R6 and VOS viewer software were used to analyze scientific knowledge map of children and literature of SCP gait. Results: After keyword search and screening, 1 364 Web of Science articles were included in a fluctuating annual volume of articles, including 65 countries / regions, 219 institutions and 200 authors; the US, Germany and Australia were high-yielding countries, and the University of Amsterdam was the leading institution; all countries and institutions had close cooperation in this field. Conclusion: SCP abnormal gait received widespread attention. Type A botox injection, baclofen intrathecal injection, nerve root cutting, and orthosis auxiliary therapy are the future spastic cerebral palsy abnormal gait research hotspots. Hospital, family-school trinity multi-center rehabilitation training is the future of children with SCP rehabilitation training direction.

目的：探讨本体感觉神经肌肉促进技术（PNF）联合运动想象疗法在脑卒中后偏瘫患者中的应用效 果。方法：随机将我院2019年12月～2022年12月104例脑卒中后偏瘫患者分为对照组和观察组各52例。 基于常规康复训练，对照组予以运动想象疗法，观察组予以PNF配合运动想象疗法，每6周为1个疗程，连续 干预2个疗程。对比2组临床疗效、改良Barthel指数（MBI）、Fugl-Meyer下肢功能量表（FMA-LE）评分、步 速、步幅、步频、膝关节与髋关节屈伸平均角速度及股四头肌、股二头肌、胫骨前肌、腓肠肌iEMC值。结果： 观察组临床治疗总有效率90.38%（47/52）高于对照组73.08%（38/52）（P＜0.05）；治疗1个、2个疗程后观察组 的MBI评分、FMA-LE评分均高于对照组（P＜0.05）；观察组治疗1个、2个疗程步速、步幅、步频及髋关节、膝 关节屈伸平均角速均大于对照组（P＜0.05）；治疗1个、2个疗程观察组股四头肌、股二头肌、胫骨前肌、腓肠 肌iEMC值大于对照组（P＜0.05）。结论：PNF联合运动想象疗法对脑卒中后偏瘫进行干预效果良好，可增 强下肢肌群肌力，改善步态特征，提升肢体功能，从而增强患者生活自理能力。

To explore the hot topics and development trends in the field of Alzheimer's disease (AD) through Mendelian randomization (MR) studies. Methods: Relevant English literature on MR studies of AD was retrieved from the Web of Science Core Collection database, spanning from the inception of the database to March 2024. CiteSpace 6.2.R4 was utilized for visual analysis of authors, countries, institutions, co-citation of documents, co-occurrence of keywords, and keyword clustering, and a knowledge map was constructed. Additionally, the PatSnap Global New Drug Intelligence Database was consulted to investigate the drug development status of biomarkers related to AD. Results: A total of 347 English articles were included after deduplication, with an increasing trend in annual publication volume. British scholar Ben-shlomo Yoav had the highest betweenness centrality. The top three countries in terms of publication volume were China, the United States, and the United Kingdom, while the top three countries in betweenness centrality were Poland, France, and Canada. China had the highest publication volume but only collaborated with the United States and the Netherlands. The top three institutions were University College London, Harvard University, and Fudan University. In the keyword clustering map, "#0 risk factors" was most closely related to AD biomarkers, with amyloid precursor protein (APP) and tau (TAU) emerging as more promising drug targets. Conclusion: MR studies on AD are mainly conducted in China, the UK, and the US. The primary research focus is on risk factors for AD onset, such as amyloid protein in cerebrospinal fluid. Related studies have identified APP and TAU as more important biomarkers and drug targets.

Alzheimer’s disease (AD) is a neurodegenerative disorder marked by progressive cognitive decline and driven by complex pathological processes, including β-amyloid deposition, hyperphosphorylated tau aggregation, and neuroinflammation. β-Hydroxybutyrate (BHB), the predominant circulating ketone body, functions not only as an alternative energy substrate to mitigate neuronal energy deficits but also acts on multiple pathological targets central to AD progression. This review systematically summarizes the neuroprotective mechanisms of BHB in AD, focusing on mitochondrial dysfunction, pathological protein deposition, neuroinflammation, oxidative stress, and insulin resistance. Clinical studies indicate that BHB significantly improves cognition in APOE ε4-negative patients, yet current strategies for inducing endogenous ketosis or supplementing exogenous ketones face substantial challenges. Future research should focus on optimizing BHB administration protocols, defining the optimal therapeutic blood concentration range, and advancing BHB as a targeted metabolic intervention for AD. Collectively, this review provides a theoretical framework for understanding the multi-mechanistic synergy of BHB in AD and its clinical translation.

As the principal afferent pathway for noxious stimuli, nociceptive sensory neurons have been shown to actively participate in tumor progression. Numerous studies indicate a complex bidirectional crosstalk between sensory neurons and tumors: tumors promote tumor innervation by releasing neurotrophic factors and axon guidance molecules, while sensory neurons remodel the tumor microenvironment by releasing neuropeptides, thereby modulating cancer proliferation, angiogenesis, immune evasion, and metastasis. However, this sensory neuro-tumor interaction exhibits marked heterogeneity across tumors of different organ origins, and its organ-specific mechanisms have yet to be systematically elucidated. Accordingly, this review aims to systematically delineate the organ-specific mechanisms by which nociceptive sensory neurons contribute to the initiation and progression of multiple solid tumors, evaluate the therapeutic potential of targeting the sensory neuron-tumor signaling axis, and provide a theoretical basis and research directions for developing organ-specific neuromodulatory strategies.

Amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder characterized by progressive motor neuron loss, currently lacks effective clinical treatments and carries an extremely poor prognosis. Recent advances in understanding ALS pathogenesis have increasingly highlighted the central role of genetic factors—particularly as most prior studies focused on high-penetrance classic genes in familial cases, leaving sporadic ALS genetic architecture largely unexplained. Risk genes typically represent small-effect genetic variants across the genome that collectively influence disease susceptibility through polygenic interactions, epigenetic modifications, and gene-environment interplay. Breakthroughs from high-throughput sequencing coupled with multi-omics technologies have identified dozens of novel ALS risk genes in recent years. Elucidating their functional mechanisms could provide crucial molecular evidence for decoding ALS heritability patterns. This review systematically summarizes molecular regulatory mechanisms of newly discovered ALS risk genes over the past five years, evaluates their potential roles in core pathogenic pathways, and emphasizes their translational potential as precision therapy targets. By integrating multi-omics datasets with gene editing tools, we aim to accelerate clinical translation of these findings—potentially transforming ALS management through personalized medicine grounded in genetic insights.

To develop a novel restraint garment for cerebrovascular interventional procedures and investigate its safety and efficacy in cerebrovascular interventional surgeries. Methods: A total of 140 patients with acute large-artery occlusive stroke undergoing mechanical thrombectomy were enrolled and divided into a trial group (n=69) and a control group (n=71). The control group utilized conventional restraint straps, while the trial group employed the novel restraint garment for cerebrovascular interventional procedures. Comparisons were made between the two groups regarding the time to first vascular recanalization, total surgical time, 30-day modified Rankin Scale (mRS) score, intraoperative limb dislodgement rate, average surgical cost per patient, and safety indicators. Results: Compared with the control group, the novel restraint garment significantly shortened the time to first vascular recanalization [(43.5±13.7) min v.s (50.7±15.7) min, P=0.039] and total surgical time [(81.1±15.6) min v.s (93.2±21.1) min, P=0.027]. The trial group also demonstrated a significantly lower rate of limb dislodgement (0% v.s 35.2% , P<0.001) and reduced average surgical cost per patient [(76 315±12 400) yuan v.s (81 462±14 142) yuan, P=0.040] compared with the control group. In terms of safety, the rate of skin redness at the restraint site in the trial group (8.7% v.s 42.3%, P<0.001) was significantly lower than that in the control group. Conclusion: The novel restraint garment for cerebrovascular interventional procedures exhibits good safety and effectively shortens surgical time, reduces the intraoperative limb dislodgement rate, and lowers the average surgical cost per patient.

To quantitatively characterize the visuo-oculomotor and vestibulo-oculomotor pathways in progressive supranuclear palsy (PSP) and Parkinson's disease (PD) using video-oculography (VOG), delineate the profile of oculomotor dysfunction in each disorder, and identify parameters with differential diagnostic value. Methods: We retrospectively analyzed vestibulo-ocular reflex suppression (VOG) data from 24 PSP patients and 48 PD patients. The data included measurements of spontaneous nystagmus, gaze holding, saccades, head-shaking test, and the vestibulo-ocular reflex suppression (VORS) test. Results: In PSP patients, the incidence of restricted vertical gaze range, decreased vertical saccadic peak velocity, saccadic hypometria and prolonged latency, horizontal gaze-evoked nystagmus (GEN), horizontal saccade hypometria and reduced velocity, as well as VORS functional abnormalities, were all significantly higher than those in PD patients (P< 0.05 for all). Spontaneous nystagmus was significantly more prevalent in PD patients than that in PSP patients (P= 0.006). The incidence of saccadic intrusions, vertical saccade hypometria, prolonged horizontal saccade latency, and perverted head-shaking nystagmus (pHSN) showed no significant difference between the PSP and PD groups (P>0.05 for all). Conclusion: Oculomotor and vestibulo-ocular assessments holds significant clinical value in differentiating PSP from PD. Specifically, vertical saccade dysfunction and VORS abnormalities serve as critical differential diagnosis indicators for distinguishing between the two conditions.

To investigate the protective effects of bilirubin on white matter injury and cognitive impairment under chronic cerebral hypoperfusion, and to elucidate its association with the regulation of microglial functional states. Methods: A bilateral common carotid artery stenosis (BCAS) mouse model was employed to induce chronic cerebral hypoperfusion. Behavioral assessments, histological analyses, and single-cell transcriptomic profiling were integrated to systematically evaluate the effects of bilirubin on white matter integrity and the inflammatory microenvironment. Results: Bilirubin treatment significantly improved learning, memory, and recognition abilities in BCAS mice, accompanied by marked attenuation of demyelination and structural disruption in the corpus callosum. Single-cell transcriptomic and histological analyses revealed that bilirubin suppressed inflammatory and immune-response-related transcriptional programs, thereby inhibiting the inflammatory and phagocytic activation of microglia. Trajectory inference and transcription factor regulatory analyses demonstrated that bilirubin redirected microglial state transitions away from inflammation-associated terminal states toward homeostatic and repair-related phenotypes. This shift was characterized by enhanced TGF-β-associated regulatory networks and concurrent suppression of interferon signaling pathways. Conclusion: Bilirubin effectively alleviates white matter injury and cognitive dysfunction induced by chronic cerebral hypoperfusion by reshaping microglial functional states and the inflammatory microenvironment.

To analyze the correlation between repetitive nerve stimulation (RNS) characteristics and the severity of myasthenia gravis (MG), and to explore its application in evaluating the efficacy of integrated traditional Chinese and Western medicine treatment for generalized myasthenia gravis (GMG). Methods: Adult GMG patients with spleen-kidney deficiency type, admitted to Wuhan Integrated Hospital of Traditional Chinese and Western Medicine from May 2021 to December 2023, were selected and randomly divided into a Western medicine group and an integrated traditional Chinese and Western medicine group. The neuro-electrophysiological characteristics of RNS in all enrolled patients were compared, including the positive rate, distribution of positive muscles, and the maximum amplitude decrement ratio of the compound muscle action potential (CMAP). The correlation between the CMAP maximum amplitude decrement ratio and the Quantitative Myasthenia Gravis Score (QMGs), the Myasthenia Gravis Activities of Daily Living (MG-ADL) scale, and the traditional Chinese medicine (TCM) symptom score in assessing GMG condition was analyzed. Changes in the CMAP maximum amplitude decrement ratio, QMGs score, MG-ADL score, and TCM symptom score before treatment, and at 3 and 6 months after treatment were compared and analyzed between the two groups. Results: A total of 74 GMG patients were enrolled, with 66 actually completing the clinical observation (35 in the Western medicine group, 31 in the integrated medicine group). Among the enrolled patients, the RNS positive rate was 81.82% to 94.44% , with no statistically significant difference in positive rates among patients of different MGFA types (P>0.05). The distribution of RNS positive muscles was consistent with the range of myasthenia involvement, showing facial nerve > accessory nerve > median nerve. As the MGFA type increased, the CMAP maximum amplitude decrement ratio showed an upward trend, but the difference was not statistically significant (P>0.05). Before treatment, and at 3 and 6 months after treatment, there was no significant correlation between the CMAP maximum amplitude decrement ratio and the QMGs score (P>0.05). Before treatment and at 6 months after treatment, there was a correlation between the CMAP maximum amplitude decrement ratio and the MG-ADL score (P<0.05). Before treatment, there was a correlation between the CMAP maximum amplitude decrement ratio and the TCM symptom score (P<0.05). After treatment, the CMAP maximum amplitude decrement ratio, QMGs score, MG-ADL score, and TCM symptom score in both groups were significantly lower than before treatment (P<0.01). Intergroup comparison results showed that at 3 and 6 months of treatment, the TCM symptom score in the integrated medicine group was lower than that in the Western medicine group (P<0.05). Conclusion: In GMG patients, the RNS positive rate is high. The CMAP maximum amplitude decrement ratio has reference significance in assessing the severity of GMG, the improvement in patients’daily living ability, and the improvement in TCM symptom scores.

目的：探讨老年急性缺血性脑卒中（acute ischemic stroke，AIS）患者血小板和淋巴细胞比值（platelet/ lymphocyte ratio，PLR）与重组组织型纤溶酶原激活剂（recombinant tissue plasminogen activator，rt-PA）静脉 溶栓后出血转化（hemorrhagic transformation，HT）及近期预后的关系。方法：选取132例老年AIS患者，收集 临床资料，行rt-PA静脉溶栓，依据静脉溶栓后是否发生HT分为HT组和非HT组，依据PLR值分为高水平 PLR（≥140.29）组和低水平PLR（＜140.29）组，并且随访90 d评定神经功能预后。比较HT组和非HT组患 者一般资料、实验室指标。Logistic回归分析老年AIS患者rt-PA静脉溶栓后发生HT的影响因素，受试者工 作特征（receiver operating characteristic，ROC）曲线分析PLR对老年AIS患者rt-PA静脉溶栓后HT的预测价 值。比较高水平PLR组和低水平PLR组患者90 d神经功能预后的差异。结果：HT组患者NIHSS评分、发 病至溶栓时间、心房颤动史、PLT、PLR均高于非HT组，LYW低于非HT组（均P＜0.05）。老年AIS患者rt-PA 静脉溶栓后HT的危险因素包括NIHSS评分、发病至溶栓时间、心房颤动及PLR。ROC曲线显示PLR预测 老年 AIS 患者 rt-PA 静脉溶栓后 HT 的截断值为 147.415，曲线下面积为 0.807，灵敏度为 76.2%，特异度为 82.9%。高水平PLR组患者90 d神经功能预后不良发生率高于低水平PLR组患者（P＜0.05）。结论：PLR是 老年AIS患者rt-PA静脉溶栓后HT的独立影响因素，对HT有较好的预测价值，并且高水平PLR可能预示其 近期神经功能预后不良。