Nature Reviews Neurology最新文献

{"title":"Intracerebral haemorrhage - mechanisms, diagnosis and prospects for treatment and prevention.","authors":"David J Seiffge, Simon Fandler-Höfler, Yang Du, Martina B Goeldlin, Wilmar M T Jolink, Catharina J M Klijn, David J Werring","doi":"10.1038/s41582-024-01035-w","DOIUrl":"https://doi.org/10.1038/s41582-024-01035-w","url":null,"abstract":"<p><p>Intracerebral haemorrhage (ICH) is a devastating condition associated with high mortality and substantial residual disability among survivors. Effective treatments for the acute stages of ICH are limited. However, promising findings from randomized trials of therapeutic strategies, including acute care bundles that target anticoagulation therapies, blood pressure control and other physiological parameters, and trials of minimally invasive neurosurgical procedures have led to renewed optimism that patient outcomes can be improved. Currently ongoing areas of research for acute treatment include anti-inflammatory and haemostatic treatments. The implementation of effective secondary prevention strategies requires an understanding of the aetiology of ICH, which involves vascular and brain parenchymal imaging; the use of neuroimaging markers of cerebral small vessel disease improves classification with prognostic relevance. Other data underline the importance of preventing not only recurrent ICH but also ischaemic stroke and cardiovascular events in survivors of ICH. Ongoing and planned randomized controlled trials will assess the efficacy of prevention strategies, including antiplatelet agents, oral anticoagulants or left atrial appendage occlusion (in patients with concomitant atrial fibrillation), and optimal management of long-term blood pressure and statin use. Together, these advances herald a new era of improved understanding and effective interventions to reduce the burden of ICH.</p>","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":" ","pages":""},"PeriodicalIF":28.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638484","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":"Altered muscle cholesterol transport in ALS","authors":"Heather Wood","doi":"10.1038/s41582-024-01029-8","DOIUrl":"10.1038/s41582-024-01029-8","url":null,"abstract":"","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"643-643"},"PeriodicalIF":28.2,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431631","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":"Lewy body pathology accelerates AD progression","authors":"Heather Wood","doi":"10.1038/s41582-024-01028-9","DOIUrl":"10.1038/s41582-024-01028-9","url":null,"abstract":"","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"643-643"},"PeriodicalIF":28.2,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431634","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":"Engineered T cells show therapeutic potential for CNS injury","authors":"Lisa Kiani","doi":"10.1038/s41582-024-01032-z","DOIUrl":"10.1038/s41582-024-01032-z","url":null,"abstract":"A study in a mouse model of spinal cord injury helps to elucidate the neuroprotective mechanisms of autoimmune T cells during the early stages of injury, which could be harnessed through T cell therapy to improve long-term outcomes.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"643-643"},"PeriodicalIF":28.2,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431632","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":"Evidence for an NMOSD prodrome","authors":"Heather Wood","doi":"10.1038/s41582-024-01030-1","DOIUrl":"10.1038/s41582-024-01030-1","url":null,"abstract":"","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"643-643"},"PeriodicalIF":28.2,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431633","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":"BCAS1+ oligodendrocytes aid remyelination in MS","authors":"Heather Wood","doi":"10.1038/s41582-024-01031-0","DOIUrl":"10.1038/s41582-024-01031-0","url":null,"abstract":"","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"643-643"},"PeriodicalIF":28.2,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431628","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":"Coeliac disease as a model for understanding multiple sclerosis","authors":"Natalia Drosu,&nbsp;Kjetil Bjornevik,&nbsp;Marianna Cortese,&nbsp;Michael Levy,&nbsp;Ludvig M. Sollid","doi":"10.1038/s41582-024-01025-y","DOIUrl":"10.1038/s41582-024-01025-y","url":null,"abstract":"The genetic architecture of multiple sclerosis (MS) is similar to that of coeliac disease, with human leukocyte antigen (HLA) being the greatest genetic determinant in both diseases. Furthermore, similar to the involvement of gluten in coeliac disease, Epstein–Barr virus (EBV) infection is now widely considered to be an important environmental factor in MS. The molecular basis for the HLA association in coeliac disease is well defined, and B cells have a clear role in antigen presentation to gluten-specific CD4+ T cells. By contrast, the mechanisms underlying the HLA association of MS are unknown but accumulating evidence indicates a similar role of B cells acting as antigen-presenting cells. The growing parallels suggest that much could be learned about the mechanisms of MS by using coeliac disease as a model. In this Perspective article, we discuss the insights that could be gained from these parallels and consider the possibility of antiviral treatment against EBV as a therapy for MS that is analogous to the gluten-free diet in coeliac disease. In this Perspective, the authors discuss how our understanding of coeliac disease could provide insights into the mechanisms of multiple sclerosis, the involvement of Epstein–Barr virus and the possibility of antiviral treatment against the virus as a therapy for multiple sclerosis.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"685-690"},"PeriodicalIF":28.2,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142384893","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":"Systemic determinants of brain health in ageing","authors":"Eric E. Smith,&nbsp;Geert Jan Biessels,&nbsp;Virginia Gao,&nbsp;Rebecca F. Gottesman,&nbsp;Arthur Liesz,&nbsp;Neal S. Parikh,&nbsp;Costantino Iadecola","doi":"10.1038/s41582-024-01016-z","DOIUrl":"10.1038/s41582-024-01016-z","url":null,"abstract":"Preservation of brain health is a worldwide priority. The traditional view is that the major threats to the ageing brain lie within the brain itself. Consequently, therapeutic approaches have focused on protecting the brain from these presumably intrinsic pathogenic processes. However, an increasing body of evidence has unveiled a previously under-recognized contribution of peripheral organs to brain dysfunction and damage. Thus, in addition to the well-known impact of diseases of the heart and endocrine glands on the brain, accumulating data suggest that dysfunction of other organs, such as gut, liver, kidney and lung, substantially affects the development and clinical manifestation of age-related brain pathologies. In this Review, a framework is provided to indicate how organ dysfunction can alter brain homeostasis and promote neurodegeneration, with a focus on dementia. We delineate the associations of subclinical dysfunction in specific organs with dementia risk and provide suggestions for public health promotion and clinical management. Peripheral organ dysfunction can have considerable effects on brain health, contributing to neurodegeneration and dementia. This Review explores how clinical and subclinical dysfunction of specific organ systems can impact brain health and discusses the implications for dementia prevention.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"647-659"},"PeriodicalIF":28.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383808","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":"Continuing evolution of migraine-specific therapies — targeting migraine with precision and persistence","authors":"Dimos D. Mitsikostas,&nbsp;Alan Rapoport","doi":"10.1038/s41582-024-01026-x","DOIUrl":"10.1038/s41582-024-01026-x","url":null,"abstract":"Treatment options for migraine have expanded rapidly over the past few years. The latest success in a phase II trial of a new class of drugs for migraine holds the promise of another alternative, with important implications for our understanding of migraine and its clinical management.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"645-646"},"PeriodicalIF":28.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383599","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":"Fluid biomarkers of chronic traumatic brain injury","authors":"Susanna Friberg,&nbsp;Caroline Lindblad,&nbsp;Frederick A. Zeiler,&nbsp;Henrik Zetterberg,&nbsp;Tobias Granberg,&nbsp;Per Svenningsson,&nbsp;Fredrik Piehl,&nbsp;Eric P. Thelin","doi":"10.1038/s41582-024-01024-z","DOIUrl":"10.1038/s41582-024-01024-z","url":null,"abstract":"Traumatic brain injury (TBI) is a leading cause of long-term disability across the world. Evidence for the usefulness of imaging and fluid biomarkers to predict outcomes and screen for the need to monitor complications in the acute stage is steadily increasing. Still, many people experience symptoms such as fatigue and cognitive and motor dysfunction in the chronic phase of TBI, where objective assessments for brain injury are lacking. Consensus criteria for traumatic encephalopathy syndrome, a clinical syndrome possibly associated with the neurodegenerative disease chronic traumatic encephalopathy, which is&nbsp;commonly associated with sports concussion, have been defined only recently. However, these criteria do not fit all individuals living with chronic consequences of TBI. The pathophysiology of chronic TBI shares many similarities with other neurodegenerative and neuroinflammatory conditions, such as Alzheimer disease. As with Alzheimer disease, advancements in fluid biomarkers represent one of the most promising paths for unravelling the chain of pathophysiological events to enable discrimination between these conditions and, with time, provide prediction modelling and therapeutic end points. This Review summarizes fluid biomarker findings in the chronic phase of TBI (≥6 months after injury) that demonstrate the involvement of inflammation, glial biology and neurodegeneration in the long-term complications of TBI. We explore how the biomarkers associate with outcome and imaging findings and aim to establish mechanistic differences in biomarker patterns between types of chronic TBI and other neurodegenerative conditions. Finally, current limitations and areas of priority for future fluid biomarker research are highlighted. Traumatic brain injury can result in long-lasting symptoms and is associated with progressive neurodegenerative and neuroinflammatory pathology, but biomarkers to diagnose and monitor these chronic effects are lacking. Here, Thelin and co-workers summarize the available evidence for fluid biomarker use in chronic traumatic brain injury.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"20 11","pages":"671-684"},"PeriodicalIF":28.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368965","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}