Nature Reviews Neurology最新文献_第5页

Moving artificial intelligence from research to real-world clinical use in neurology 将人工智能从研究转移到神经病学的实际临床应用。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-29 DOI: 10.1038/s41582-026-01225-8

James T. Teo, Arman Eshaghi, Mark P. Richardson, Lara Jehi, Sandor Beniczky

{"title":"Moving artificial intelligence from research to real-world clinical use in neurology","authors":"James T. Teo, Arman Eshaghi, Mark P. Richardson, Lara Jehi, Sandor Beniczky","doi":"10.1038/s41582-026-01225-8","DOIUrl":"10.1038/s41582-026-01225-8","url":null,"abstract":"Artificial intelligence (AI) applications in neurology have reached an inflection point. Despite US Food and Drug Administration approval of numerous algorithms in neuroimaging, neurophysiology, genetics and chatbots, their real-world impact remains limited. This disconnect between research promise and clinical reality represents a gap in understanding how to translate AI algorithms into clinical benefit for patients globally. In this Perspective, we examine the challenges that prevent clinical AI use in neurology moving beyond pilot studies towards meaningful clinical impact. We consider the steps required in the process of translation, including research, validation of AI models, regulatory approval pathways and clinical implementation. We discuss implementation of AI models as stand-alone products versus embedded platforms, and the requirements for sustainable deployment. Beyond traditional clinical decision support tools, we examine paraclinical applications of AI, including chatbots and ambient voice documentation. We recommend expanding capacity for prospective validation and scaling by implementing and validating technologies across multiple sites and countries, which requires infrastructure from long-term partnerships. Neurology must shift from asking whether AI can work to understanding how to use it safely at scale. Numerous artificial intelligence (AI) applications are being developed in neurology, but their real-world impact remains limited. In this Perspective, Teo et al. examine the challenges that prevent clinical AI use in neurology moving beyond pilot studies towards meaningful clinical impact.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 8","pages":"498-506"},"PeriodicalIF":31.2,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348912","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}

引用次数: 0

Adaptive deep brain stimulation in Parkinson disease: clinical implementation and outlook 适应性脑深部刺激治疗帕金森病：临床实施与展望。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-29 DOI: 10.1038/s41582-026-01239-2

Esther Florin, Andrea A. Kühn

引用次数: 0

Artificial intelligence in headache care 头痛护理中的人工智能。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-28 DOI: 10.1038/s41582-026-01226-7

Anker Stubberud

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Artificial intelligence could reshape research and care in disorders of consciousness 人工智能可以重塑意识障碍的研究和护理。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-27 DOI: 10.1038/s41582-026-01229-4

Anna Estraneo, Erika Molteni

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Bo Peng: microglia replacement therapy from bench to bedside 博鹏：小胶质细胞替代疗法从实验室到床边

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-23 DOI: 10.1038/s41582-026-01237-4

Lisa Kiani, Bo Peng

引用次数: 0

Varun Venkataramani: the rise of cancer neuroscience Varun Venkataramani：癌症神经科学的兴起

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-23 DOI: 10.1038/s41582-026-01240-9

Lisa Kiani, Varun Venkataramani

引用次数: 0

Christina Kim: functional and biochemical mapping of neural circuits 克里斯蒂娜·金：神经回路的功能和生化制图

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-23 DOI: 10.1038/s41582-026-01236-5

Lisa Kiani, Christina K. Kim

引用次数: 0

Failed resolution of inflammation in intracerebral haemorrhage 脑出血中炎症消退失败。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-23 DOI: 10.1038/s41582-026-01227-6

Liang Cao, Wang Zhao, Yanjun Zhang, Wenjun Pi, V. Wee Yong, Mengzhou Xue

{"title":"Failed resolution of inflammation in intracerebral haemorrhage","authors":"Liang Cao, Wang Zhao, Yanjun Zhang, Wenjun Pi, V. Wee Yong, Mengzhou Xue","doi":"10.1038/s41582-026-01227-6","DOIUrl":"10.1038/s41582-026-01227-6","url":null,"abstract":"Intracerebral haemorrhage (ICH) is a subtype of stroke, with resulting long-term disability determined by secondary brain injury. The prevailing biphasic model of neuroinflammation, which conceptualizes a temporal transition from acute to chronic stages, fails to reconcile persistent clinical trial failures or to explain the mechanisms underpinning the progression to chronic neurological deficits. We propose that the core pathology is the failure of acute inflammation to resolve in a timely manner owing to a functional collapse of physiological pro-resolution programmes, governed by dysregulation at critical molecular checkpoints such as the USP11–p53 axis. This failure locks the microenvironment into a destructive, non-resolving state, perpetuating immune-mediated damage. We discuss the evidence for a causal link between this checkpoint failure and the defining chronic sequelae: progressive white matter injury, inhibitory gliosis and large-scale network disconnection. We conceptualize the long-term motor, cognitive and affective impairments as a cohesive clinical entity, which we term post-ICH sequelae. This framework calls for a therapeutic reorientation from broad immunosuppression towards precision pro-resolution strategies such as USP11 inhibitors guided by biomarker-based immune staging. This Perspective provides a theoretical foundation, currently supported predominantly by preclinical evidence, and a translational roadmap for improving long-term recovery after ICH. Intracerebral haemorrhage is associated with long-term disability determined by secondary brain injury. In this Perspective, the authors propose that failed resolution of inflammation is the key driver of the chronic effects, leading to progressive white matter injury, inhibitory gliosis and large-scale network disconnection.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 8","pages":"507-518"},"PeriodicalIF":31.2,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148305063","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}

引用次数: 0

Narcolepsy is (not) an autoimmune disease 嗜睡症是（不是）自身免疫性疾病。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-19 DOI: 10.1038/s41582-026-01232-9

Anne Vassalli, Mehdi Tafti, Roland S. Liblau

{"title":"Narcolepsy is (not) an autoimmune disease","authors":"Anne Vassalli, Mehdi Tafti, Roland S. Liblau","doi":"10.1038/s41582-026-01232-9","DOIUrl":"10.1038/s41582-026-01232-9","url":null,"abstract":"Narcolepsy type 1 (NT1) is a chronic disease characterized by excessive daytime sleepiness and cataplexy. NT1 often strikes at a young age, severely impairing quality of life, and is frequently underdiagnosed or misdiagnosed. NT1 is tightly linked to deficiency in the wake-promoting and state-stabilizing hypocretin (HCRT) neuropeptides, which are produced by a small group of hypothalamic neurons. Given its strong association with the HLA-DQB1*06:02 allele, NT1 is widely assumed to result from autoimmune destruction of HCRT neurons. However, whether autoreactive immune responses represent a cause or a consequence of the disease remains an open question, and immune-mediated pathogenic mechanisms distinct from autoimmune cell killing are being explored. The observation that genes highly expressed in the hypothalamus, including HCRT, are epigenetically altered in post-mortem brain tissue from patients with NT1 has led to an alternative model whereby immune-triggered HCRT gene silencing, rather than HCRT neuron degeneration, causes HCRT deficiency. In this Perspective, we critically appraise the autoimmune and epigenetic models and their therapeutic implications and consider whether they can be reconciled. Narcolepsy type 1 (NT1), a chronic disease characterized by excessive daytime sleepiness and cataplexy, is widely assumed to result from autoimmune destruction of hypocretin (HCRT)-expressing neurons. However, as discussed in this Perspective, an alternative epigenetic model is emerging whereby immune-triggered HCRT gene silencing causes HCRT deficiency in people with NT1.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 8","pages":"519-531"},"PeriodicalIF":31.2,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148284087","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}

引用次数: 0

Ten years of disease-modifying therapy in spinal muscular atrophy: lessons learned and future directions 脊髓性肌萎缩症的十年疾病改善疗法：经验教训和未来方向。

IF 31.2 1区医学

Nature Reviews Neurology Pub Date : 2026-06-17 DOI: 10.1038/s41582-026-01224-9

Eugenio Mercuri, Richard S. Finkel, Francesco Muntoni

{"title":"Ten years of disease-modifying therapy in spinal muscular atrophy: lessons learned and future directions","authors":"Eugenio Mercuri, Richard S. Finkel, Francesco Muntoni","doi":"10.1038/s41582-026-01224-9","DOIUrl":"10.1038/s41582-026-01224-9","url":null,"abstract":"Spinal muscular atrophy (SMA) is an autosomal recessive disease caused by deletions or mutations in the SMN1 gene, leading to loss of motor neurons with subsequent muscle atrophy and weakness. The disease is characterized by progression in weakness and loss of function that is only partially reduced by improved standards of care. The advent of three new therapies has dramatically changed the natural history of all SMA subtypes, including the severe and advanced type I SMA. As the first drug was approved in 2016, these therapies have been available for a decade, with a rapidly increasing collection of data demonstrating their safety and efficacy in a range of clinical trials and in the real-world setting. We critically review how the field has evolved in response to the new therapies, the long-term follow-up and the emergence of new phenotypes, and the outcome of initiating these therapies in presymptomatic individuals identified via newborn screening programmes. We also review the challenges related to the interpretation of long-term outcomes once placebo-control data end, as well as the difficulties in making decisions and interpreting the results of sequential and combinatorial therapies. Finally, we review the evolution of the existing therapies, such as intrathecal gene therapy instead of its intravenous administration, or the higher dose intrathecal antisense oligonucleotide nusinersen, and new therapeutic approaches currently being studied in clinical trials. A decade after the first disease-modifying therapy was approved for spinal muscular atrophy, transforming the disease outlook, the field continues to evolve in response to real-world evidence, emerging phenotypes and new therapeutic strategies. This Review examines the challenges and opportunities presented by long-term outcomes, newborn screening and the emergence of sequential and combinatorial treatment approaches.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 9","pages":"549-563"},"PeriodicalIF":31.2,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272048","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}

引用次数: 0