Brain最新文献

{"title":"Motor recovery through perineuronal net modulation in a Parkinson’s disease mouse model","authors":"David Benacom, Camille Chataing, Alain Prochiantz, Ariel A Di Nardo","doi":"10.1093/brain/awaf226","DOIUrl":"https://doi.org/10.1093/brain/awaf226","url":null,"abstract":"Perineuronal nets are specialized extracellular matrix structures forming preferentially around parvalbumin interneurons to regulate plasticity. While cortical perineuronal nets have been implicated in sensory plasticity and memory modulation, perineuronal nets of the primary motor cortex have been largely overlooked. We found that transient reduction of primary motor cortex perineuronal nets by ChABC treatment in otherwise healthy adult mice resulted in temporary deficits in motor function. In a mouse model of Parkinson's disease based on unilateral 6-hydroxydopamine lesions of the midbrain, perineuronal net levels were decreased in both primary motor cortex hemispheres 2 weeks post-lesion, yet returned to baseline within 5 weeks. We discovered that subsequent transient reduction of primary motor cortex perineuronal nets through ChABC treatment could unlock motor recovery when coupled with motor stimulation. This recovery was associated with a bilateral increase in perineuronal-net-enwrapped parvalbumin interneurons and a rebalancing of parvalbumin cell soma excitatory synaptic markers. These findings reveal distinct roles of perineuronal net plasticity – first in response to the initial midbrain lesion and then during rescue after ChABC treatment – suggesting that primary motor cortex perineuronal nets play a nuanced role in regulating motor function. This duality positions perineuronal nets as potential therapeutic targets for motor rehabilitation strategies in Parkinson's disease.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"12 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulants for disorders of consciousness in the intensive care unit: a randomized, placebo-controlled trial","authors":"Marwan H Othman, Attila Géry Toury-Puel, Karen Irgens Tanderup Hansen, Moshgan Amiri, Pardis Zarifkar, Costanza Peinkhofer, Sarah Gharabaghi Stückler, Markus Harboe Olsen, Jens Bjerregaard, Margit Smitt, Anna Søgaard Magnussen, Axel Forsse, Jacob Møller, Marie Katrine Klose Nielsen, Cecilie Høgfeldt Jessen, Christian Hassager, Simon Hyttel-Sørensen, Anders Perner, Morten Hylander Møller, Peter Hasse Møller-Sørensen, John Hauerberg, Peter Birkeland, Sigurdur Thor Sigurdsson, Christian Aage Wamberg, Theis Skovsgaard Itenov, Christian S Meyhoff, Kirsten Møller, Tobias S Andersen, Jesper Kjaergaard, Daniel Kondziella","doi":"10.1093/brain/awaf228","DOIUrl":"https://doi.org/10.1093/brain/awaf228","url":null,"abstract":"In the intensive care unit (ICU), management of unresponsive patients with brain injury focuses on preventing secondary brain damage. Therapeutic strategies that directly promote the recovery of consciousness are urgently needed. In an investigator-initiated, randomized, placebo-controlled, double-blind, cross-over trial, we studied the effects of apomorphine and methylphenidate in ICU patients with acute disorders of consciousness (DoC). We hypothesized that these stimulants would improve consciousness biomarkers assessed by automated pupillometry (primary outcome) and clinical signs of consciousness (secondary outcome). We randomized 50 ICU patients with DoC (14 women; mean age 63 ± 10 years; 48 with non-traumatic brain injuries) to strata consisting of three consecutive treatment sessions during which apomorphine, methylphenidate or placebo were administered. In total, we administered 112 study medications, including 36 doses of apomorphine, 39 doses of methylphenidate and 37 doses of placebo. Missing administrations were due to death, ICU discharge, or spontaneous consciousness recovery. Plasma concentrations of stimulants confirmed drug exposure. We found no adverse events related to the trial drugs. Pupillometry recordings of sufficient quality (n = 590) were available from 48 (96%) patients. A pupillary response to a verbal arithmetic command (i.e., ≥3 pupillary dilations on five verbal arithmetic tasks) was identified during 70 (12%) of these recordings. Seven (15%) patients without any other observable response to spoken commands also passed a stricter threshold of ≥4 pupillary dilations, suggesting cognitive motor dissociation. Apomorphine (OR 1.35, 95% CI: 0.93 to 1.96) and methylphenidate (OR 1.29, 95% CI: 0.89 to 1.86) did not significantly increase pupillary responses. However, after study drug administration, 10 (20%) patients showed improved clinical arousal at least once. Signs of arousal were noted after one dose of placebo, four doses of apomorphine (OR 5.04, 95% CI: 0.56 to 120.7), and seven doses of methylphenidate (OR 9.96, 95% CI: 1.36 to 235.8). Changes toward higher consciousness level categories were observed once after placebo, four times after apomorphine (OR 5.67, 95% CI 0.63 to 169.46), and three times after methylphenidate (OR 3.41, 95% CI 0.34 to 88.00). In a post-hoc analysis, patients with greater pupillary responsiveness showed better arousal, suggesting that this condition may predict stimulant drug effects. In conclusion, while pupillometry revealed no direct drug effects on overall pupillary responses, stimulants may have triggered clinical arousal in some patients, particularly in those with greater pupillary responsiveness. These findings require replication but should guide future pharmacological trials aimed at improving consciousness recovery after brain injury.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"26 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering DST-associated disorders: biallelic variants affecting DST-b cause a congenital myopathy.","authors":"Maureen Jacob, Heike Kölbel, Philip Harrer, Robert Kopajtich, Pinki Munot, Melanie T Achleitner, Susann Badmann, Melanie Brugger, Theresa Brunet, Gisèle Bonne, Marta Codina, Laura Ebner, Peyman Eshraghi, Katharina Eyring, Ahmad Shah Farhat, René G Feichtinger, Elisabeth Graf, Anna Marcé-Grau, Andreas Hahn, Henry Houlden, Ehsan Ghayoor Karimiani, Véronique Manel, Katharina Mayerhanser, Juliette Nectoux, Isabelle Nelson, Rahul Phadke, Holger Prokisch, Saeid Sadeghian, Alice Saparov, Anne Schänzer, Ulrike Schara-Schmidt, Julia Schmidt, Rahel Schuler, Caroline Sewry, Gholamreza Shariati, Silke Slanz, Dmitrii Smirnov, Rivka Sukenik-Halevy, Homa Tajsharghi, Mehran Beiraghi Toosi, Laura Trujillano, Joachim Weis, Louise C Wilson, Rabah Ben Yaou, Mina Zamani, Michael Zech, Jana Zschüntzsch, Uwe Kornak, David Goméz-Andrés, Reza Maroofian, Juliane Winkelmann, Andreas Roos, Felix Distelmaier, Johannes A Mayr, Matias Wagner","doi":"10.1093/brain/awaf227","DOIUrl":"https://doi.org/10.1093/brain/awaf227","url":null,"abstract":"<p><p>Dystonin (DST) encodes three major isoforms, DST-a, DST-b, and DST-e. Biallelic pathogenic variants in DST have previously been associated with two allelic monogenic disorders: Hereditary Sensory and Autonomic Neuropathy type VI (caused by a loss of DST-a) and Epidermolysis bullosa simplex 3 (caused by a loss of DST-e). We investigated patients diagnosed with congenital myopathy using exome or genome sequencing. In 19 affected individuals from 14 unrelated families, we identified nine different variants in biallelic state located in exons 40-41, specific to DST-b. Affected individuals presented with severe neonatal myopathy characterized by arthrogryposis, hypotonia, and dilated cardiomyopathy. Postnatal CPAP ventilation was required in nine patients, and seven died within the first three years of life. Survivors showed an improvement of symptoms, with the oldest three patients, now over 25 years old, exhibiting normal cognition and being ambulatory. RNA analyses demonstrated that transcripts encoding DST-b are predominantly expressed in skeletal muscle, heart tissue, and cultured fibroblasts, but not in brain matching the phenotypic spectrum. Patient-derived fibroblasts exhibited reduced DST mRNA expression. Proteomic analysis confirmed a reduction of DST protein levels due to an absence of the DST-b isoform. Muscle biopsies from four patients aged 1 month to 3 years revealed mild, non-specific myopathic changes. Ultrastructural analysis in three individuals showed mild and focal myofibrillar disruption and non-specific undulating nuclear membranes, with these changes observed in two cases each. Additionally, we identified two homozygous variants affecting both DST-a and DST-b isoforms in four patients from two unrelated families; all presented with severe arthrogryposis and died intrauterine or shortly after birth. Genotype-Phenotype correlation in these patients and previously published cases with respective variants resulted in the definition of a DST-associated lethal congenital contracture syndrome. Our findings demonstrate that biallelic variants exclusively affecting DST-b cause an autosomal recessive congenital myopathy. Variants that also impact DST-a besides DST-b result in a more severe, lethal congenital contracture syndrome. The location of the variant within DST allows for phenotype prediction. We propose redefining DST as a disease-associated gene linked to four distinct allelic disease phenotypes.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"POU3F2 regulates canonical Wnt signalling via SOX13 and ADNP to expand the neural progenitor population","authors":"Courtney R Benoit, Lilia B Sattler, Aimee J Aylward, Olivia Pembridge, Bella Kim, Christina R Muratore, Meichen Liao, Amy He, Nancy Ashour, Seeley B Fancher, Alexandra M Lish, Richard V Pearse, Joseph D Buxbaum, Tracy L Young-Pearse","doi":"10.1093/brain/awaf221","DOIUrl":"https://doi.org/10.1093/brain/awaf221","url":null,"abstract":"Loss-of-function mutations in the transcription factor POU3F2 have been identified in individuals with neurodevelopmental disorders. To elucidate the mechanistic role of POU3F2 in human neurodevelopment, we induced POU3F2 disruption in human neural progenitor cells (NPCs). Mutation of POU3F2 in NPCs causes reduced baseline canonical Wnt signalling and decreased proliferation, resulting in premature specification of radial glia. Additionally, POU3F2 levels across genetically diverse NPCs significantly associate positively with baseline canonical Wnt signalling and negatively with markers of radial glia specification. Through a series of unbiased analyses, we show that SOX13 and ADNP are transcriptional targets of POU3F2 which mediate POU3F2’s effects on Wnt signalling in human NPCs. Finally, we describe five individuals with autism spectrum disorder that harbor loss-of-function mutations in POU3F2, enhancing the genetic evidence for its critical role in human neurodevelopment. Together, these studies define POU3F2 as an activator of canonical Wnt signalling and mechanistically link two high-confidence autism genes, ADNP and POU3F2, in the regulation of neurodevelopment.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"9 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disentangling epilepsy and dementia: more to do, together","authors":"Arjune Sen","doi":"10.1093/brain/awaf225","DOIUrl":"https://doi.org/10.1093/brain/awaf225","url":null,"abstract":"This scientific commentary refers to ‘The association of seizure control with neuropathology in dementia’ by Zawar et al. (https://doi.org/10.1093/brain/awaf017).","PeriodicalId":9063,"journal":{"name":"Brain","volume":"10 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disease spectrum and long-term prognosis of patients with BAG3-associated neuromuscular diseases in Europe","authors":"Gorka Fernández-Eulate, Cyril Gitiaux, Simone Thiele, Heinz Jungbluth, Anna Potulska-Chromik, Chiara Marini-Bettolo, Jean Baptiste Davion, Germán Morís, Eduard Gallardo, Montsé Olivé, Carlos Pablo de Fuenmayor-Fernández de la Hoz, Frederique Audic, Arnaud Isapof, Maggie C Walter, Corrado Angelini, Enrico Bertini, Ulrike Schara-Schmidt, Kristl G Claeys, Maike F Dohrn, Mohamed Dembele, Frederic Fer, Guy Brochier, Teresinha Evangelista, Anna Kostera-Pruszczyk, Shahram Attarian, Volker Straub, Cristina Dominguez-Gonzalez, John Vissing, Pascale Richard, Corinne Metay, Diala Khraiche, Karim Wahbi, Tanya Stojkovic","doi":"10.1093/brain/awaf223","DOIUrl":"https://doi.org/10.1093/brain/awaf223","url":null,"abstract":"De novo or autosomal dominant BAG3 gene variants cause a wide range of skeletal and cardiac muscle diseases encompassing Charcot–Marie–Tooth disease, myofibrillar myopathy, cardiomyopathy or a combination of them. Given the severity and rarity of BAG3-neuromuscular diseases (NMD), series of patients are lacking. Our aim was to characterize the clinical and genetic spectrum as well as the natural history of BAG3-NMD in Europe. In this multicentre retrospective study, we collected clinical, ancillary, and genetic data of patients with NMD and BAG3 variants, identified from European paediatric and adult neuromuscular reference centres from May to December 2023 following a call circulated through the European Reference Network EURO-NMD and other partners. Responses were received from 35 centres in 17 countries. Twenty-six patients (65.4% males, 34.6% females) with BAG3-NMD from 18 different families were included in the study. The c.626C&amp;gt;T p.(Pro209Leu) variant, carried by 16 patients, was the only recurrent variant and was associated with a homogeneous and severe phenotype, with predominantly lower-limb motor weakness (n=13, 81.25%) or heart failure (n=3, 18.75%) as the presenting feature, and a mean age at symptom onset of 7.8±3.4 years. Where available (n=13), electroneuromyography showed a polyneuropathy with demyelinating features and a frequently associated myopathy. Eleven (68.8%) patients had restrictive cardiomyopathy on initial assessment. Orthopaedic manifestations were common, with contractures (n=15, 93.8%), foot deformities (n=11, 84.6%), and scoliosis and/or rigid spine (n=12, 80%). At last follow-up (age 21.5±8.6 years), of the patients carrying the p.(Pro209Leu) variant, 10 (62.5%) had lost ambulation, 14 (93.3%) had respiratory insufficiency (11 requiring ventilation), and 12 (75%) had a restrictive cardiomyopathy, leading to heart failure and heart transplantation in five and four patients, respectively. Eight (50%) patients died prematurely at a mean age of 22.5±9.6 years, most frequently from sudden death (n=5). The other 10 patients carried three other BAG3 variants, and showed a milder disease course, with all patients remaining ambulatory, without cardiorespiratory manifestations at last follow-up. The p.(Arg309*) nonsense variant, known to cause isolated dilated cardiomyopathy, as well as the p.(Val505Glyfs*6) frameshift variant resulting in a premature stop codon, caused distal hereditary motor neuropathy. This is the largest study of patients with BAG3-NMD, delineating the frequency, specific presentation, and the natural history in patients with the recurrent BAG3 p.(Pro209Leu) missense variant, crucial for informing patient management in the context of a rapidly progressive disease. All other BAG3 variants were rare and caused milder clinical presentations.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"25 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding the phenotype of SORD mutation.","authors":"Roxane Pruvost, Arnaud Bruneel, Nicolas Dochez, Grégory Kuchcinski, Vianney Poinsignon, Céline Tard","doi":"10.1093/brain/awaf216","DOIUrl":"https://doi.org/10.1093/brain/awaf216","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extending the role of neurofilament light in multiple sclerosis beyond measuring irreversible neurodegeneration","authors":"Nick G Cunniffe","doi":"10.1093/brain/awaf224","DOIUrl":"https://doi.org/10.1093/brain/awaf224","url":null,"abstract":"This scientific commentary refers to ‘Markers of axonal injury in blood and tissue triggered by acute and chronic demyelination’ by Abdelhak et al. (https://doi.org/10.1093/brain/awaf144).","PeriodicalId":9063,"journal":{"name":"Brain","volume":"20 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of DOT1L disrupts neuronal transcription and leads to a neurodevelopmental disorder","authors":"Marissa J Maroni, Melissa Barton, Katherine Lynch, Ashish R Deshwar, Philip D Campbell, Josephine Millard, Rachel Lee, Annastelle Cohen, Rili Ahmad, Alekh Paranjapye, Víctor Faundes, Gabriela M Repetto, Caoimhe McKenna, Amelle L Shillington, Chanika Phornphutkul, Hanne B Hove, Grazia M S Mancini, Rachel Schot, Tahsin Stefan Barakat, Christopher M Richmond, Julie Lauzon, Ahmed Ibrahim Elsayed Ibrahim, Caroline Nava, Delphine Héron, Minke M A van Aalst, Slavena Atemin, Mila Sleptsova, Iliyana Aleksandrova, Albena Todorova, Debra L Watkins, Mariya A Kozenko, Daniel Natera-de Benito, Carlos Ortez, Berta Estevez-Arias, François Lecoquierre, Kévin Cassinari, Anne-Marie Guerrot, Jonathan Levy, Xenia Latypova, Alain Verloes, A Micheil Innes, Xiao-Ru Yang, Siddharth Banka, Katharina Vill, Maureen Jacob, Michael Kruer, Peter Skidmore, Carolina I Galaz-Montoya, Somayeh Bakhtiari, Jessica L Mester, Michael Granato, Karim-Jean Armache, Gregory Costain, Erica Korb","doi":"10.1093/brain/awaf212","DOIUrl":"https://doi.org/10.1093/brain/awaf212","url":null,"abstract":"Individuals with monoallelic gain-of-function variants in the histone lysine methyltransferase DOT1L display global developmental delay and varying congenital anomalies. However, the impact of monoallelic loss of DOT1L remains unclear. Here, we sought to define the effects of partial DOT1L loss by applying bulk and single-nucleus RNA-sequencing, ChIP-sequencing, imaging, multielectrode array recordings, and behavioral analysis of zebrafish and multiple mouse models. We present a cohort of 16 individuals (12 females, 4 males) with neurodevelopmental disorders and monoallelic DOT1L variants, including a frameshift deletion, an in-frame deletion, a nonsense, and missense variants clustered in the catalytic domain. We demonstrate that specific variants cause loss of methyltransferase activity. In primary cortical neurons, Dot1l knockdown disrupts transcription of synaptic genes, neuron branching, expression of a synaptic protein, and neuronal activity. Further in the cortex of heterozygous Dot1l mice, Dot1l loss causes sex-specific transcriptional responses and H3K79me2 depletion, including within down-regulated genes. Lastly using both zebrafish and mouse models, we found behavioral disruptions that include developmental deficits and sex-specific social behavioral changes. Overall, we define how DOT1L loss leads to neurological dysfunction by demonstrating that partial Dot1l loss impacts neuronal transcription, neuron morphology, and behavior across multiple models and systems.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"10 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From signal to senescence: IFNγ drives muscle atrophy in myositis","authors":"Werner Stenzel, Hans-Hilmar Goebel, Marie Holzer","doi":"10.1093/brain/awaf220","DOIUrl":"https://doi.org/10.1093/brain/awaf220","url":null,"abstract":"This scientific commentary refers to ‘Interferon-g causes myogenic cell dysfunction and senescence in immune myopathies’ by Hou et al. (https://doi.org/10.1093/brain/awaf153).","PeriodicalId":9063,"journal":{"name":"Brain","volume":"21 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144237704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}