MOVEMENT DISORDERS运动障碍
MOVEMENT DISORDERS(英文缩写 MOVEMENT DISORD),ISSN 0885-3185,eISSN 1531-8257,中文译名:运动障碍 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.698 | Q1 |
| 2022 | 8.600 | Q1 |
| 2023 | 7.400 | Q1 |
| 2024 | 7.600 | Q1 |
| 2025 | 7.700 | Q1 |
MOVEMENT DISORDERS 最新收录文献
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1. 2026 International Congress of Parkinson's Disease and Movement Disorders.
1. 2026年国际帕金森病与运动障碍大会PMID:日期:2026-10该文献暂无摘要。
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3. Does a Timing-Specific Effect Establish Hyperdirect Pathway Recruitment?
3. 特定时序效应是否确立了超直接通路的招募？PMID:日期:2026-09-29该文献暂无摘要。
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4. Multilevel Structure-Function Coupling Reveals Network Signatures of Remission in Paroxysmal Kinesigenic Dyskinesia.
4. 多层级结构-功能耦合揭示发作性运动诱发性运动障碍缓解期的网络特征PMID:日期:2026-09-24Paroxysmal kinesigenic dyskinesia (PKD) causes brief, movement-triggered dystonic or choreic attacks that can severely affect daily life. Though most patients eventually remit, timing and rate of improvement differ substantially across individuals, and predictive biomarkers remain lacking. Evidence indicates that PKD reflects distributed network dysfunction. To investigate how structural wiring supports or constrains these dysfunctions, as evaluated by structure-function (structural connectivity-functional connectivity [SC-FC]) coupling. Diffusion kurtosis imaging and resting-state functional magnetic resonance imaging (fMRI) were obtained in 95 patients with PKD and 44 healthy controls (HC). SC-FC coupling was quantified at nodal, intranetwork, and internetwork levels. Patients were classified as remission or nonremission. Machine-learning classifiers based on multilevel SC-FC features were trained to distinguish PKD from HCs and to predict remission status. Associations between SC-FC features and disease duration were assessed using Spearman's correlation. Patients with PKD exhibited widespread SC-FC coupling abnormalities consistent with distributed rather than focal network dysfunction. Remission and nonremission subgroups exhibited distinct SC-FC signatures, centering on cerebellar, somatomotor, and default-mode systems. Machine-learning classifiers discriminated PKD patients from HCs (area under the receiver operating characteristic curve [AUC] = 0.91) and remission from nonremission patients (AUC = 0.95). Cerebellar-default-mode network coupling was the top discriminative feature and correlated positively with disease duration (Spearman's r = 0.26, P = 0.031, FDR corrected). Multilevel SC-FC coupling analyses reveal systems-level abnormalities in PKD and suggest that partial normalization of coupling patterns accompanies remission. Cerebellar-default-mode network coupling may serve as a sensitive imaging biomarker of remission status and disease progression, highlighting coupling-based metrics as candidates for predicting PKD trajectory. © 2026 International Parkinson and Movement Disorder Society.
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5. Association Between Long-Term Exposure to Air Pollution and Parkinson's Disease: Administrative Cohort of Older Adults in South Korea.
5. 长期暴露于空气污染与帕金森病之间的关联：韩国老年人行政队列研究PMID:日期:2026-09-23Evidence regarding the association between long-term exposure to ambient air pollution and Parkinson's disease (PD) remains inconsistent, particularly among older adults in Asian populations. We aimed to examine the association between long-term exposure to ambient air pollutants and incident PD in a nationwide administrative cohort of older adults in South Korea. We analyzed 5.3 million adults aged ≥65 years from the Korean National Health Insurance Database (2010-2019). Incident PD was ascertained using nationwide insurance claims data, requiring hospitalization or repeated outpatient diagnoses. District-level annual concentrations of fine particulate matter (PM), nitrogen dioxide (NO), and ozone (O) were estimated using the Community Multiscale Air Quality model. Time-varying Cox proportional hazards models were used to estimate hazard ratios (HRs) per interquartile range (IQR) increase in a 1-year moving-average exposure, adjusting for individual- and district-level covariates. During follow-up, 143,557 PD cases were identified. In fully adjusted models, each IQR increase in PM (4.3 μg/m) and O (7.3 ppb) was associated with a modestly increased PD incidence (PM: HR = 1.018, 95% CI: 1.008-1.028; O: HR = 1.019, 95% CI: 1.006-1.033). However, NO showed an inverse association after full adjustment. Effect modification by demographic or clinical characteristics was not statistically significant. Long-term exposure to PM and O was associated with a small but statistically significant increase in PD incidence among older adults in Korea. These findings are consistent with a possible association between air pollution and the etiology of neurodegenerative diseases, although effect sizes were modest and should be interpreted with caution. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
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7. Cross-Ethnic Replication of Intersectin-1 as a Parkinson's Disease Susceptibility Gene in a Large Chinese Cohort.
7. 在中国大型队列中交叉族群验证Intersectin-1作为帕金森病易感基因PMID:日期:2026-09-22Rare loss-of-function (LoF) variants in Intersectin-1 (ITSN1) have recently been identified as strong genetic risk factors for Parkinson's disease (PD) in individuals of European ancestry. The aim was to determine whether this association extends to other populations. We analyzed whole-exome sequencing data from 2063 unrelated Chinese patients with PD and performed rare-variant burden analyses together with 3298 controls and publicly available East Asian reference datasets. Gene-based association was evaluated using optimized sequence kernel association test (SKAT-O) for rare LoF variants and predicted damaging missense variants. Three previously unreported frameshift LoF variants were identified in the patients, all of which were absent from controls and classified as likely pathogenic. Gene-based burden analyses demonstrated enrichment of rare deleterious ITSN1 variants in patients with PD across multiple control datasets, supporting the contribution of ITSN1 to PD susceptibility. Our findings provide the first independent evidence supporting the association between rare ITSN1 variants and PD in an East Asian population, extending previous discoveries from European cohorts. The identification of population-specific pathogenic variants further refines the genetic architecture of ITSN1 and reinforces its role as a cross-population susceptibility gene for PD. © 2026 International Parkinson and Movement Disorder Society.
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8. ATXN8OS Intermediate Expansion Acts as a Genetic Modifier in Spinocerebellar Ataxia Type 48 (SCA48/STUB1).
PMID:日期:2026-09-21Association between monoallelic STUB1 variant and expanded ATXN8OS alleles was recently reported, suggesting a pathogenic interaction that may influence spinocerebellar ataxia type 48 (SCA48) phenotype. We investigated the frequency and clinical impact of ATXN8OS in a large cohort of STUB1 carriers compared to individuals with other ataxias and controls. Ataxic individuals and controls from the SPATAX/BIOMOV cohorts (Paris Brain Institute) were screened for ATXN8OS and other CAG expansions using polymerase chain reaction (PCR)/repeat-prime PCR (RP-PCR) and ExpansionHunter. STUB1 carriers underwent whole-genome or exome sequencing. Our cohort comprised 12 biallelic STUB1 carriers (SCAR16) and 67 monoallelic STUB1 carriers (SCA48) without other causative variants. ATXN8OS expansions (84-177 CTA/CTG repeats) were identified in seven SCA48 individuals (10.5%) who exhibited earlier onset (median age 28 vs. 47 years, P < 0.001) compared to other SCA48 individuals but with similar clinical presentation. ATXN8OS expansions were also found in two healthy controls older than 50 years (2/286, 0.7%) and in eight index cases with autosomal dominant ataxia (8/400, 2%), including four carrying another molecular diagnosis without any effect on the phenotype. Other intermediate expansions were identified in individuals with SCA48: seven (10.5%) carried intermediate TBP alleles (40-46 CAG/CAA) without any effect on dementia prevalence; four carried intermediate HTT alleles (28-29 CAG); and three carried intermediate ATXN1 expansions (38 CAG). ATXN8OS intermediate expansion acts as a genetic modifier in SCA48 but not in other ataxias. Moreover, expanded intermediate alleles in neurodegenerative disease genes were present in one-third of SCA48 individuals. These alleles may increase polyglutamine burden, potentially saturating STUB1 E3 ubiquitin ligase activity. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
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9. Striatal Dopaminergic Reserve Shapes the Longitudinal Impact of Peripheral Immune Activation on Motor Progression in Parkinson's Disease.
9. 纹状体多巴胺能储备塑造外周免疫激活对帕金森病运动进展的纵向影响PMID:日期:2026-09-21Peripheral immune dysregulation has been implicated in Parkinson's disease (PD) progression, but whether motor deterioration reflects accelerated nigrostriatal degeneration or residual dopaminergic reserve remains unclear. To examine whether baseline and time-varying neutrophil-to-lymphocyte ratio (NLR) relate to motor progression and striatal dopamine transporter (DAT) decline, and whether baseline DAT modifies the NLR-motor relationship. We analyzed 7 years of Parkinson's Progression Markers Initiative (PPMI) data from 335 drug-naive patients with PD and 305 healthy controls. Linear mixed-effects models assessed NLR trajectories, longitudinal Unified Parkinson's Disease Rating Scale-Part III (UPDRS-III) and DAT associations, and moderation by baseline DAT; follow-up motor assessments were ON-medication. NLR remained higher in PD than controls (P < 0.001). A 1 SD higher baseline NLR was associated with an additional 0.350 UPDRS-III points/year (P < 0.001), while higher-than-usual visit-wise NLR was associated with higher concurrent motor severity (β = 0.352, P = 0.041). Neither baseline nor time-varying NLR was consistently associated with DAT decline. Higher baseline DAT binding moderated NLR-related motor progression in the left caudate (β = 0.326, P < 0.001), right caudate (β = 0.183, P = 0.036), and left putamen (β = 0.168, P = 0.023); within the DAT-imaging interval, moderation persisted in the left caudate (β = 0.314, P = 0.044) and left putamen (β = 0.223, P = 0.047). Higher baseline NLR predicted faster treated-state motor worsening, while visit-wise NLR tracked concurrent severity. These associations were not accompanied by clear evidence of accelerated DAT decline, supporting a reserve-dependent relationship between peripheral inflammation and motor progression. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
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10. Urine-Derived Neuronal Extracellular Vesicle α-Synuclein Seed Amplification Assay for Synucleinopathies: A Non-Invasive Biomarker Study.
10. 尿液来源神经元细胞外囊泡α-突触核蛋白种子扩增检测用于突触核蛋白病：一项无创生物标志物研究PMID:日期:2026-09-21α-Synuclein aggregation is a pathological hallmark of synucleinopathies, including Parkinson's disease (PD) and multiple system atrophy (MSA). Although pathogenic α-synuclein seeds can be detected by real-time quaking-induced conversion (RT-QuIC), current assays primarily rely on cerebrospinal fluid, whose invasiveness limits repeated and large-scale applications. We therefore evaluated the feasibility of detecting pathogenic α-synuclein using urine-derived neuronal extracellular vesicles (NEVs). Urine-derived NEVs were enriched by direct immunoprecipitation using L1CAM-conjugated magnetic beads. The RT-QuIC assay was performed in 26 patients with PD, 13 with MSA, and 25 disease controls, including 16 healthy controls (HC), 4 with progressive supranuclear palsy (PSP), and 5 with normal pressure hydrocephalus (NPH). Urine-derived NEVs exhibited characteristic neuronal and exosomal markers and a typical extracellular vesicle size distribution. The urine-based RT-QuIC assay distinguished PD from disease controls with 73.1% sensitivity and 84% specificity, and MSA from disease controls with 76.9% sensitivity and 84% specificity. When compared with HC alone, sensitivity and specificity were 73.1% and 93.8% for PD, and 76.9% and 93.8% for MSA, respectively. Kinetic analysis showed higher maximum fluorescence intensity and area under the curve (AUC) in PD compared with both disease controls and HC (P < 0.001 in all). MSA also demonstrated higher maximum fluorescence intensity than HC and increased AUC compared with both disease controls and HC (P < 0.05 in all). We developed and optimized a completely non-invasive urine-derived NEV α-synuclein RT-QuIC assay that demonstrates high specificity and moderate sensitivity for synucleinopathies. This approach warrants further validation in larger cohorts. © 2026 International Parkinson and Movement Disorder Society.