ANNALS OF NEUROLOGY神经病学年鉴
ANNALS OF NEUROLOGY(英文缩写 ANN NEUROL),ISSN 0364-5134,eISSN 1531-8249,中文译名:神经病学年鉴 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 | 11.274 | Q1 |
| 2022 | 11.200 | Q1 |
| 2023 | 8.100 | Q1 |
| 2024 | 7.700 | Q1 |
| 2025 | 7.500 | Q1 |
ANNALS OF NEUROLOGY 最新收录文献
-
1. Associations Between Prediagnosis Plasma Neurofilament Light Polypeptide and Amyotrophic Lateral Sclerosis Risk in the Danish EPIC Cohort.
1. 丹麦EPIC队列中诊断前血浆神经丝轻链多肽与肌萎缩侧索硬化症风险之间的关联PMID:日期:2026-10-02Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a rapid time from symptoms onset to diagnosis. Elevated neurofilament light polypeptide (NfL) is well-established in symptomatic ALS and up to 5 years prediagnosis, but earlier timeframes remain understudied. We aimed to assess plasma NfL levels up to 23 years before ALS diagnosis and the relation to ALS risk. We conducted a nested matched case-control study within the Danish EPIC cohort (baseline 1993-1997) including 166 ALS cases (diagnosed 1997-2017) and 332 controls matched on birth year and sex. Plasma samples collected 0.4 to 23.2 years (median 14.1 years) prediagnosis were analyzed for NfL using Olink Target 96. Odds ratios were estimated using conditional logistic regression. Discriminatory performance was evaluated using receiver operating characteristic curves. NfL levels were elevated in ALS cases relative to controls up to 14.6 years before diagnosis. Among those with blood samples collected <5, 5 to 14.6, and >14.6 years before diagnosis, the odds ratios (95% CI) for ALS per standard deviation increase in the normalized protein expression value of NfL were 3.8 (1.4-10.3), 1.7 (1.2-2.3), and 1.3 (0.9-1.7), respectively. The areas under the curve for ALS discrimination by NfL among those with blood collected <5 and 5-14.6 years before diagnosis were 0.78 and 0.63, respectively. Plasma NfL elevation may occur significantly earlier than previously reported, indicating a much longer ALS prodrome. Assuming other biomarker changes may also occur earlier, this raises the possibility of identifying at-risk individuals early that could benefit epidemiologic analyses, clinical trials, and prevention efforts. ANN NEUROL 2026.
-
2. Memory and Plasma pTau217 Refine Prognosis in Down Syndrome.
2. 记忆与血浆pTau217优化唐氏综合征的预后评估PMID:日期:2026-10-02Individuals with Down syndrome (DS) are at high risk for Alzheimer's disease (AD), yet accessible tools for routine clinical screening of AD in individuals with DS remain limited. Using data from the Alzheimer Biomarker Consortium-Down Syndrome (ABC-DS), we show that integrating plasma pTau217 with performance on the modified cued recall task identifies a subgroup of cognitively stable individuals at markedly elevated risk of developing clinical impairment in the next 7 years. This low-burden, multimodal framework improves prognosis, supports more informed clinical management and efficient trial enrichment in Down syndrome. ANN NEUROL 2026.
-
3. The Making of Women Leaders in Academic Neurology.
3. 学术神经病学领域女性领导者的培养PMID:日期:2026-09-30该文献暂无摘要。
-
4. Biallelic PIGB Variants Cause Motor Neuropathy with Conduction Blocks and Peripheral Nerve Hyperexcitability.
4. 双等位基因PIGB变异导致伴有传导阻滞和外周神经过度兴奋的运动神经病PMID:日期:2026-09-30Glycosylphosphatidylinositol (GPI)-anchored proteins play critical roles in nervous system function. Pathogenic variants in genes involved in GPI-anchor biosynthesis cause early-onset multisystem disorders known as inherited GPI deficiencies. We describe a novel neuromuscular phenotype associated with PIGB deficiency. Patients with neuromuscular disease carrying PIGB variants were identified, and clinical data collected. GPI-anchored protein and free-GPI expression were assessed by flow cytometry and variants validated in a PIGB knockout cellular model. Biallelic PIGB variants were identified in 12 patients (median age 32 years, range 15-52 years) from 9 independent families. Of 15 variants, 13 were novel, including a de novo inversion generating a PIGB::RAB27A gene fusion. Of 12 patients, 10 presented with distal lower-limb weakness, and neurophysiological studies demonstrated a motor-predominant neuropathy with frequent conduction blocks in all patients. Signs of nerve hyperexcitability were observed in 9 patients, with electromyography neuromyotonic discharges and myokymia compatible with peripheral nerve hyperexcitability in 6. A total of 3 patients showed a decremental response on repetitive nerve stimulation; 2 were symptomatic and responded to pyridostigmine, consistent with neuromuscular junction transmission defect. Neurodevelopmental features were inconsistent. Flow cytometry revealed variable reductions of GPI-anchored proteins, but consistent reduction of free GPI in blood cells. Novel variants impaired GPI-anchor expression in vitro. We expand the phenotypic spectrum of inherited GPI deficiencies with a novel neuromuscular syndrome encompassing motor neuropathy with conduction blocks, peripheral nerve hyperexcitability, and occasional neuromuscular junction defects associated with PIGB variants. PIGB and other GPI-anchor biosynthesis genes should be considered in motor neuropathy with conduction blocks. ANN NEUROL 2026.
-
5. Reframing the Gut-Brain Axis: The Gut Wall as a Neural Immune Interface in Multiple Sclerosis and Autoimmune Neurological Diseases.
5. 重构肠-脑轴：在多发性硬化症和自身免疫性神经系统疾病中，肠壁作为神经免疫界面PMID:日期:2026-09-26Gut wall physiology in multiple sclerosis (MS) and autoimmune neurologic diseases remains underexplored. This review examines gut wall dysfunctions' contribution to MS and autoimmune neurological disorder pathogenesis and progression. We discuss 3 inter-related aspects of gut physiology: intestinal barrier, enteric nervous system (ENS), and mucosal immunity. We highlight the ENS as a putative target of immune injury in selected antibody-mediated and T cell-associated neurologic diseases. Finally, we propose a unifying framework in which the gut functions as a site of immune priming and target of autoimmune injury, bridging microbiome-driven mechanisms in MS with ENS-directed autoimmunity across neurologic diseases. ANN NEUROL 2026.
-
6. Association Between Genetic Ancestry and Multiple Sclerosis Severity.
6. 遗传祖先与多发性硬化症严重程度之间的关联PMID:日期:2026-09-25The objective of this study was to determine whether genetic ancestry is associated with differences in the clinical course of multiple sclerosis (MS). Participants with MS living in the United Kingdom >18 years old were recruited from 2021 to 2025 and genotyped from saliva using a commercial array. Genetic ancestry was inferred using a random forest classifier trained on a diverse reference dataset. Participant-reported MS characteristics including the Age-Related Multiple Sclerosis Severity Score (ARMSS) and age at MS diagnosis were ascertained at recruitment. We analyzed data from 816 people with MS (pwMS), comprising 260 people of South Asian ancestry (31.9%), 163 of African ancestry (20.0%), 316 of European ancestry (38.7%), and 77 participants from other backgrounds. The included cohort was predominantly female (72.3% women), diagnosed with MS at a median age of 32 years (interquartile range [IQR] = 14.0) and recruited at a median age of 44.6 years (IQR = 18.2). Neither South Asian nor African ancestry was consistently associated with higher MS severity compared with European-ancestry participants. No genetic variants were associated with MS severity at genomewide statistical significance. In this cross-sectional, diverse, UK cohort, neither South Asian nor African ancestry is associated with greater MS-related disability. These findings argue against a genetic basis for the previously observed differences between MS outcomes when contrasting ethnic groups. ANN NEUROL 2026.
-
8. Sensitivity of Non-contrast Computed Tomography Net Water Uptake Versus FLAIR-MRI, with MR-DWI Reference Standard, for Early Detection and Physiological Characterization of Ischemic Edema in Hyperacute Stroke.
PMID:日期:2026-09-23On non-contrast computed tomography (NCCT), progressive hypoattenuation can be quantified as percent net water uptake (%NWU), whereas relative fluid attenuated inversion recovery (rFLAIR)-magnetic resonance imaging hyperintensity marks later-stage vasogenic edema and blood-brain-barrier disruption. We compared the degree and rate of %NWU versus rFLAIR development and characterized 4 ischemic edema imaging profiles relative to a magnetic resonance (MR)-diffusion-weighted-imaging (MR-DWI) reference standard. NCCT and fluid attenuated inversion recovery (FLAIR) images from MR-DWI-positive hyperacute stroke patients were visually rated positive (+) or negative (-) for ischemic hypodensity/hyperintensity and sulcal-effacement (SE), defining 4 edema imaging profiles: (I) NWU-/FLAIR-/SE-, (II) NWU+/FLAIR-/SE-, (III) NWU+/FLAIR+/SE-, and (IV) NWU+/FLAIR+/SE+. %NWU, rFLAIR, and relative apparent diffusion coefficient (rADC) were quantified within the DWI/apparent diffusion coefficient-defined core region-of-interest, normalized to the contralateral mirror region, and compared between groups. Of 53 DWI+ patients, n = 5/17/13/17 were in groups I to IV, with mean onset-to-CT times of 2.4 ± 1.2/2.5 ± 1.6/3.2 ± 1.9/5.0 ± 1.6 hours (p < 0.01), and baseline characteristics were comparable (all p ≥ 0.12). Mean %NWU differed between all groups (1.4 ± 0.3/4.3 ± 4.2/8.0 ± 4.1/13.6 ± 4.3; all pairwise p < 0.012), rADC did not (p = 0.21), and rFLAIR differed only between groups II and III versus group IV (p = 0.02, p = 0.04). %NWU and rFLAIR were uncorrelated (R = 0.02, p = 0.48). Fitted %NWU increased monotonically and near-linearly within 4.5 hours post-ictus, whereas rFLAIR rose abruptly only in the late transition to group IV. Quantitative %NWU-CT was more sensitive than rFLAIR for detecting the earliest edematous stages of hyperacute stroke, discriminating early, intermediate, late, and late-severe (SE) stages; rFLAIR increased only in the latest stage. %NWU may, therefore, provide a practical, quantitative CT marker of edema progression, supporting acute triage and risk phenotyping in CT-first pathways, pending prospective validation. ANN NEUROL 2026.
-
9. Deep Inspiration Clarifies a Web-Like Vertebral Artery Defect.
9. 深吸气使网样椎动脉缺损变得清晰PMID:日期:2026-09-22该文献暂无摘要。
-
10. Growth Differentiation Factor 15 as a Cerebrospinal Fluid Biomarker for the Diagnosis and Prognosis of Leptomeningeal Metastasis.
10. 生长分化因子15作为脑脊液生物标志物用于软脑膜转移的诊断和预后PMID:日期:2026-09-22As leptomeningeal metastasis (LM) has a poor prognosis, reliable cerebrospinal fluid (CSF) diagnostic biomarkers are urgently needed. This study evaluated the diagnostic value of CSF growth differentiation factor 15 (GDF15) in LM from lung adenocarcinoma (LUAD) and breast cancer (BC). A cohort of 726 CSF samples, including those from patients with LUAD LM, LUAD without LM (LUAD Non-LM; comprising LUAD without brain metastasis and LUAD with parenchymal brain metastasis), neurological controls, and patients with primary intracranial solid tumors, as well as a BC cohort of 83 CSF samples from BC LM and BC Non-LM patients, were enrolled in the study. The GDF15 and carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) levels were measured by the chemiluminescence method. CSF GDF15 levels were elevated >25-fold in LUAD LM compared with Non-LM and neurological controls. CSF GDF15 excellently discriminated LUAD LM from Non-LM (AUC 0.959 and 0.912) and neurological controls (AUC 0.975 and 0.929) in 2 independent cohorts. CSF GDF15 levels effectively distinguished LUAD LM from parenchymal brain metastasis (AUC 0.954) and primary intracranial solid tumors (AUC 0.950). High CSF GDF15 levels were associated with shorter overall survival in LUAD LM patients. CSF CEACAM6 similarly differentiated LUAD LM from parenchymal brain metastasis (AUC 0.956) and primary intracranial solid tumors (AUC 0.970). In the BC cohort, GDF15 (AUC 0.899) and CEACAM6 (AUC 0.869) both performed well in distinguishing LM from Non-LM. The combination of GDF15 and CEACAM6 outperformed either biomarker alone in diagnosis of LUAD LM and BC LM. CSF GDF15 is a high-performance diagnostic biomarker for LUAD LM and BC LM. ANN NEUROL 2026 ANN NEUROL 2026.