Pub Date : 2025-10-24DOI: 10.1038/s41582-025-01153-z
Iris-Katharina Penner, Matthias Grothe, Andrew Chan
Fatigue is a severely disabling symptom that can substantially impair quality of life and employment prospects, and has serious socioeconomic consequences. Different individual and disease-related variables interact to generate this complex symptom, leading to clinical heterogeneity. We currently lack a common understanding and definition of fatigue and its origins, thereby impeding professional exchange among disciplines regarding diagnosis and underlying pathophysiology. To aid the development of a common language that encapsulates the heterogeneity of fatigue, we propose a taxonomy consisting of neurogenic, myogenic and systemic clusters. Each cluster comprises the same five distinct concepts and their phenotypic expression. The interplay between multifactorial pathophysiological mechanisms might vary between diseases and over time, and additional factors such as comorbidities can modulate fatigue. Understanding this complexity is essential to improve both the diagnostic process and the development of targeted therapeutic interventions. In this Review, we compare the clinical and pathophysiological characteristics of a range of neurological and non-neurological diseases within predefined clusters of fatigue origin. We propose an integrative model for fatigue of different origin and over time based on the interplay of genetics and epigenetics, immunological changes, structural and functional brain abnormalities, and behavioural alterations. Large research consortia will be required to tackle the methodological shortcomings that currently hamper our understanding of fatigue and to initiate large longitudinal cohort studies with multidimensional readouts to further explore and address this burdensome symptom. Fatigue is a burdensome symptom that is commonly encountered in people with neurological or non-neurological diseases, but it is poorly understood and lacks a common definition and conceptualization. This Review presents new a conceptual model of fatigue that is designed to improve communication between experts from different methodological and medical backgrounds.
{"title":"Fatigue: a common but poorly understood symptom in neurological and non-neurological diseases","authors":"Iris-Katharina Penner, Matthias Grothe, Andrew Chan","doi":"10.1038/s41582-025-01153-z","DOIUrl":"10.1038/s41582-025-01153-z","url":null,"abstract":"Fatigue is a severely disabling symptom that can substantially impair quality of life and employment prospects, and has serious socioeconomic consequences. Different individual and disease-related variables interact to generate this complex symptom, leading to clinical heterogeneity. We currently lack a common understanding and definition of fatigue and its origins, thereby impeding professional exchange among disciplines regarding diagnosis and underlying pathophysiology. To aid the development of a common language that encapsulates the heterogeneity of fatigue, we propose a taxonomy consisting of neurogenic, myogenic and systemic clusters. Each cluster comprises the same five distinct concepts and their phenotypic expression. The interplay between multifactorial pathophysiological mechanisms might vary between diseases and over time, and additional factors such as comorbidities can modulate fatigue. Understanding this complexity is essential to improve both the diagnostic process and the development of targeted therapeutic interventions. In this Review, we compare the clinical and pathophysiological characteristics of a range of neurological and non-neurological diseases within predefined clusters of fatigue origin. We propose an integrative model for fatigue of different origin and over time based on the interplay of genetics and epigenetics, immunological changes, structural and functional brain abnormalities, and behavioural alterations. Large research consortia will be required to tackle the methodological shortcomings that currently hamper our understanding of fatigue and to initiate large longitudinal cohort studies with multidimensional readouts to further explore and address this burdensome symptom. Fatigue is a burdensome symptom that is commonly encountered in people with neurological or non-neurological diseases, but it is poorly understood and lacks a common definition and conceptualization. This Review presents new a conceptual model of fatigue that is designed to improve communication between experts from different methodological and medical backgrounds.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"706-720"},"PeriodicalIF":33.1,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145357687","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}
Pub Date : 2025-10-08DOI: 10.1038/s41582-025-01158-8
Lisa Kiani
Cerebellar pathology in people with type 1 spinal muscular atrophy (SMA) might contribute to motor and social communication impairments associated with the disease, according to a recent study published in Brain.
{"title":"Cerebellar pathology in spinal muscular atrophy","authors":"Lisa Kiani","doi":"10.1038/s41582-025-01158-8","DOIUrl":"10.1038/s41582-025-01158-8","url":null,"abstract":"Cerebellar pathology in people with type 1 spinal muscular atrophy (SMA) might contribute to motor and social communication impairments associated with the disease, according to a recent study published in Brain.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"592-592"},"PeriodicalIF":33.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246614","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}
Pub Date : 2025-10-07DOI: 10.1038/s41582-025-01157-9
Lisa Kiani
Autologous haematopoietic stem cell transplantation (AHSCT) offers effective therapy for people with multiple sclerosis (MS), according to new real-world data.
{"title":"Real-world effectiveness of stem cell transplantation for multiple sclerosis","authors":"Lisa Kiani","doi":"10.1038/s41582-025-01157-9","DOIUrl":"10.1038/s41582-025-01157-9","url":null,"abstract":"Autologous haematopoietic stem cell transplantation (AHSCT) offers effective therapy for people with multiple sclerosis (MS), according to new real-world data.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"591-591"},"PeriodicalIF":33.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241002","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}
Pub Date : 2025-10-07DOI: 10.1038/s41582-025-01156-w
Lisa Kiani
Glioblastomas can shift glucose metabolism from tricarboxylic acid cycle (TCA) oxidation and neurotransmitter synthesis to growth-promoting pathways, according to new research published in Nature.
{"title":"Glioblastomas divert glucose to promote growth","authors":"Lisa Kiani","doi":"10.1038/s41582-025-01156-w","DOIUrl":"10.1038/s41582-025-01156-w","url":null,"abstract":"Glioblastomas can shift glucose metabolism from tricarboxylic acid cycle (TCA) oxidation and neurotransmitter synthesis to growth-promoting pathways, according to new research published in Nature.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"591-591"},"PeriodicalIF":33.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240963","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}
Pub Date : 2025-10-01DOI: 10.1038/s41582-025-01150-2
Heather Wood
A new study presented at the 2025 American Neurological Association Annual Meeting indicates that area postrema syndrome in people with neuromyelitis optica spectrum disorder is related to elevated levels of the gut hormone glucagon-like peptide 1 and its receptor GLP-1R.
{"title":"GLP-1 is implicated in area postrema syndrome in people with NMOSD","authors":"Heather Wood","doi":"10.1038/s41582-025-01150-2","DOIUrl":"10.1038/s41582-025-01150-2","url":null,"abstract":"A new study presented at the 2025 American Neurological Association Annual Meeting indicates that area postrema syndrome in people with neuromyelitis optica spectrum disorder is related to elevated levels of the gut hormone glucagon-like peptide 1 and its receptor GLP-1R.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"591-591"},"PeriodicalIF":33.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203664","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}
Pub Date : 2025-10-01DOI: 10.1038/s41582-025-01149-9
Heather Wood
A new meta-analysis presented at the 2025 American Neurological Association Annual Meeting shows that initiation of hormone replacement therapy in women soon after the onset of menopause is associated with a reduced risk of Alzheimer disease.
{"title":"Timing of hormone replacement therapy could influence Alzheimer disease risk","authors":"Heather Wood","doi":"10.1038/s41582-025-01149-9","DOIUrl":"10.1038/s41582-025-01149-9","url":null,"abstract":"A new meta-analysis presented at the 2025 American Neurological Association Annual Meeting shows that initiation of hormone replacement therapy in women soon after the onset of menopause is associated with a reduced risk of Alzheimer disease.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"590-590"},"PeriodicalIF":33.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203876","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}
Pub Date : 2025-10-01DOI: 10.1038/s41582-025-01142-2
Saranna Fanning, Dennis Selkoe
On the basis of extensive mechanistic research over three decades, Parkinson disease (PD) and related synucleinopathies have been proposed to be combined proteinopathies and lipidopathies. Evidence strongly supports a physiological and pathogenic interplay between the disease-associated protein α-synuclein and lipids, with a demonstrable role for lipids in modulating PD phenotypes in the brain. Here, we refine this hypothesis by proposing PD to be a disease specifically involving metabolic dysregulation of fatty acids, a ‘fatty acidopathy’. We review extensive findings from many laboratories supporting the perspective that PD centres on fatty acid dyshomeostasis — alterations in the fatty acid-ome — as the critical feature of lipid aberration in PD and other α-synucleinopathies. This construct places transient α-synuclein binding to fatty acid side chains of cytoplasmic vesicles as a principal contributor to the biology of PD-relevant α-synuclein–membrane interactions. We propose that α-synuclein–fatty acid interactions in the fatty acid-rich brain are interdependent determinants of the gradual progression from neuronal health to PD, with attendant therapeutic implications. This Perspective centres on alterations in the fatty acid-ome as the critical feature of lipid aberration in α-synucleinopathies, specifically Parkinson disease. Here, the authors explain the biological and genetic basis for their hypothesis, with an emphasis on the transient binding of α-synuclein to fatty acids of various lipids.
{"title":"Parkinson disease is a fatty acidopathy","authors":"Saranna Fanning, Dennis Selkoe","doi":"10.1038/s41582-025-01142-2","DOIUrl":"10.1038/s41582-025-01142-2","url":null,"abstract":"On the basis of extensive mechanistic research over three decades, Parkinson disease (PD) and related synucleinopathies have been proposed to be combined proteinopathies and lipidopathies. Evidence strongly supports a physiological and pathogenic interplay between the disease-associated protein α-synuclein and lipids, with a demonstrable role for lipids in modulating PD phenotypes in the brain. Here, we refine this hypothesis by proposing PD to be a disease specifically involving metabolic dysregulation of fatty acids, a ‘fatty acidopathy’. We review extensive findings from many laboratories supporting the perspective that PD centres on fatty acid dyshomeostasis — alterations in the fatty acid-ome — as the critical feature of lipid aberration in PD and other α-synucleinopathies. This construct places transient α-synuclein binding to fatty acid side chains of cytoplasmic vesicles as a principal contributor to the biology of PD-relevant α-synuclein–membrane interactions. We propose that α-synuclein–fatty acid interactions in the fatty acid-rich brain are interdependent determinants of the gradual progression from neuronal health to PD, with attendant therapeutic implications. This Perspective centres on alterations in the fatty acid-ome as the critical feature of lipid aberration in α-synucleinopathies, specifically Parkinson disease. Here, the authors explain the biological and genetic basis for their hypothesis, with an emphasis on the transient binding of α-synuclein to fatty acids of various lipids.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"642-655"},"PeriodicalIF":33.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203663","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}
Pub Date : 2025-09-22DOI: 10.1038/s41582-025-01139-x
Lisa Rahm, Melissa A. Hale, Renée H. L. Raaijmakers, Alexandra Marrero Quiñones, Tejal Patki, Nicholas E. Johnson, Hans van Bokhoven, Karlien Mul
Myotonic dystrophy type 1 (DM1) is the most prevalent muscular dystrophy in adulthood and is one of the most clinically diverse monogenic diseases. Although it is classified as a neuromuscular disease, DM1 is a multisystem disorder that affects nearly all organ systems, particularly skeletal and smooth muscles, the central nervous system and the heart. Its phenotypic variability extends beyond a continuum of severity, encompassing differences in age of onset and organ involvement. DM1 is caused by a trinucleotide (CTG) repeat expansion within the 3′ untranslated region of the DMPK gene, leading to a toxic RNA gain-of-function mechanism that disrupts RNA splicing, causing widespread cellular dysfunction. Despite progress in understanding DM1 pathogenesis, gaps remain in elucidating genotype–phenotype correlations, genetic modifiers and mechanisms that influence disease progression. Breakthroughs in the past five to ten years have uncovered important insights into the molecular underpinnings of DM1 and accelerated therapeutic innovation. Targeted interventions such as small molecules, antisense oligonucleotides and gene-editing technologies are progressing into clinical trials. Additionally, emerging research on somatic instability, epigenetic modifications and novel biomarkers suggests approaches for precision medicine. This Review synthesizes recent clinical and molecular discoveries, highlighting implications for therapy development. By integrating clinical heterogeneity with mechanistic insights, we provide a framework for future translational research and therapeutic innovation in this life-limiting disease. Myotonic dystrophy type 1 (DM1) is the most prevalent muscular dystrophy in adulthood and among the most clinically diverse monogenic diseases. This Review summarizes the latest insights into the molecular underpinnings of DM1, highlighting the implications for therapy development.
{"title":"Myotonic dystrophy type 1: clinical diversity, molecular insights and therapeutic perspectives","authors":"Lisa Rahm, Melissa A. Hale, Renée H. L. Raaijmakers, Alexandra Marrero Quiñones, Tejal Patki, Nicholas E. Johnson, Hans van Bokhoven, Karlien Mul","doi":"10.1038/s41582-025-01139-x","DOIUrl":"10.1038/s41582-025-01139-x","url":null,"abstract":"Myotonic dystrophy type 1 (DM1) is the most prevalent muscular dystrophy in adulthood and is one of the most clinically diverse monogenic diseases. Although it is classified as a neuromuscular disease, DM1 is a multisystem disorder that affects nearly all organ systems, particularly skeletal and smooth muscles, the central nervous system and the heart. Its phenotypic variability extends beyond a continuum of severity, encompassing differences in age of onset and organ involvement. DM1 is caused by a trinucleotide (CTG) repeat expansion within the 3′ untranslated region of the DMPK gene, leading to a toxic RNA gain-of-function mechanism that disrupts RNA splicing, causing widespread cellular dysfunction. Despite progress in understanding DM1 pathogenesis, gaps remain in elucidating genotype–phenotype correlations, genetic modifiers and mechanisms that influence disease progression. Breakthroughs in the past five to ten years have uncovered important insights into the molecular underpinnings of DM1 and accelerated therapeutic innovation. Targeted interventions such as small molecules, antisense oligonucleotides and gene-editing technologies are progressing into clinical trials. Additionally, emerging research on somatic instability, epigenetic modifications and novel biomarkers suggests approaches for precision medicine. This Review synthesizes recent clinical and molecular discoveries, highlighting implications for therapy development. By integrating clinical heterogeneity with mechanistic insights, we provide a framework for future translational research and therapeutic innovation in this life-limiting disease. Myotonic dystrophy type 1 (DM1) is the most prevalent muscular dystrophy in adulthood and among the most clinically diverse monogenic diseases. This Review summarizes the latest insights into the molecular underpinnings of DM1, highlighting the implications for therapy development.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 11","pages":"623-641"},"PeriodicalIF":33.1,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117156","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}
Pub Date : 2025-09-22DOI: 10.1038/s41582-025-01136-0
Thomas Wirth, Jennifer Faber, Christel Depienne, Emmanuel Roze, Jérôme Honnorat, Wassilios G. Meissner, Paola Giunti, Christine Tranchant, Thomas Klockgether, Mathieu Anheim
Sporadic late-onset cerebellar ataxia (SLOCA) is a syndrome defined by subacute or chronic and progressive ataxia occurring after the age of 40 years in individuals without a family history of ataxia. The 2022 publication of revised consensus diagnostic criteria for multiple system atrophy and the emergence of promising biomarkers provides a thorough diagnostic framework that now enables the diagnosis of numerous acquired causes of SLOCA, including autoimmune disorders and neurodegenerative diseases. The ongoing development and increased availability of DNA sequencing technology have uncovered several molecular causes of SLOCA besides spastic paraplegia type 7 and very late-onset Friedreich ataxia. These additional causes include sporadic genetic disorders, such as spinocerebellar atrophy type 27B, caused by GAA expansion in the FGF14 gene, and cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS), caused by biallelic expansions in the RFC1 gene. This Review presents an updated clinical approach to the diagnosis and management of SLOCA that focuses on the most important developments in this field. Future challenges are also discussed, including the identification of additional missing genetic causes of SLOCA, especially via the use of long-read genome sequencing, improvements in SLOCA prognostication and the implementation of clinical trials of neuroprotective interventions. Many autoimmune and genetic causes of sporadic late-onset cerebellar ataxia (SLOCA) can now be identified, but some individuals remain categorized as having idiopathic SLOCA. Wirth and colleagues discuss advanced genomic techniques that might identify additional ‘missing’ SLOCA causes, potential prognostic biomarkers and progress towards effective treatments.
{"title":"Progress and challenges in sporadic late-onset cerebellar ataxias","authors":"Thomas Wirth, Jennifer Faber, Christel Depienne, Emmanuel Roze, Jérôme Honnorat, Wassilios G. Meissner, Paola Giunti, Christine Tranchant, Thomas Klockgether, Mathieu Anheim","doi":"10.1038/s41582-025-01136-0","DOIUrl":"10.1038/s41582-025-01136-0","url":null,"abstract":"Sporadic late-onset cerebellar ataxia (SLOCA) is a syndrome defined by subacute or chronic and progressive ataxia occurring after the age of 40 years in individuals without a family history of ataxia. The 2022 publication of revised consensus diagnostic criteria for multiple system atrophy and the emergence of promising biomarkers provides a thorough diagnostic framework that now enables the diagnosis of numerous acquired causes of SLOCA, including autoimmune disorders and neurodegenerative diseases. The ongoing development and increased availability of DNA sequencing technology have uncovered several molecular causes of SLOCA besides spastic paraplegia type 7 and very late-onset Friedreich ataxia. These additional causes include sporadic genetic disorders, such as spinocerebellar atrophy type 27B, caused by GAA expansion in the FGF14 gene, and cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS), caused by biallelic expansions in the RFC1 gene. This Review presents an updated clinical approach to the diagnosis and management of SLOCA that focuses on the most important developments in this field. Future challenges are also discussed, including the identification of additional missing genetic causes of SLOCA, especially via the use of long-read genome sequencing, improvements in SLOCA prognostication and the implementation of clinical trials of neuroprotective interventions. Many autoimmune and genetic causes of sporadic late-onset cerebellar ataxia (SLOCA) can now be identified, but some individuals remain categorized as having idiopathic SLOCA. Wirth and colleagues discuss advanced genomic techniques that might identify additional ‘missing’ SLOCA causes, potential prognostic biomarkers and progress towards effective treatments.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"687-705"},"PeriodicalIF":33.1,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117157","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}
In the 2024 revisions of the McDonald criteria for diagnosis of multiple sclerosis (MS), dissemination in time is no longer required. This paradigm shift is the result of advances in understanding of MS and the development of other biomarkers, enabling earlier diagnosis and treatment that will ultimately improve long-term outcomes.
{"title":"A paradigm shift away from dissemination in time in multiple sclerosis","authors":"Agustín Pappolla, Georgina Arrambide, Xavier Montalban","doi":"10.1038/s41582-025-01138-y","DOIUrl":"10.1038/s41582-025-01138-y","url":null,"abstract":"In the 2024 revisions of the McDonald criteria for diagnosis of multiple sclerosis (MS), dissemination in time is no longer required. This paradigm shift is the result of advances in understanding of MS and the development of other biomarkers, enabling earlier diagnosis and treatment that will ultimately improve long-term outcomes.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"657-658"},"PeriodicalIF":33.1,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077897","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}
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