Pub Date : 2025-12-03DOI: 10.1038/s41582-025-01163-x
Panteleimon Oikonomou, Fahimeh H. Akhoundi, Nahid Olfati, Irene Litvan
Cognitive impairment in people with Parkinson disease (PD) imposes a substantial societal burden: PD affects over 1% of the population aged 65 years and older, and 24–31% of individuals with this condition develop dementia and another 26% present with mild cognitive impairment. Given the increasing prevalence of PD in light of an ageing population, the challenge of PD-associated cognitive impairment is likely to intensify. In this Review, we highlight the latest research advances in PD-associated cognitive impairment, emphasizing emerging mechanistic insights and new biomarkers. We outline the epidemiology and natural history of cognitive decline in PD, focusing on prodromal stages and the closely related spectrum of Lewy body dementia. We discuss key pathophysiological factors and mechanisms, including aggregation and prion-like propagation of α-synuclein; co-pathologies; synaptic dysfunction; genetics; neuroinflammation; mitochondrial dysfunction; oxidative stress; microbiome alterations; degeneration of cholinergic and monoaminergic systems; autonomic dysfunction; altered neuronal network activity; and glymphatic impairment. We consider how advances in fluid and neuroimaging biomarkers, together with preclinical disease models and pathological studies, are providing insights into these mechanisms. A deeper understanding of the multifaceted pathophysiology of PD-associated cognitive impairment will help us to explain the heterogeneity of cognitive profiles and disease progression in PD, providing a foundation for personalized disease-modifying treatments. Cognitive impairment is one of a range of non-motor symptoms that people with Parkinson disease (PD) can experience in addition to the hallmark motor symptoms of the disease. In this Review, Oikonomou et al. outline the epidemiology and natural history of cognitive decline in PD and related disorders, and discuss the key underlying pathophysiological factors and mechanisms.
{"title":"Characteristics and mechanisms of cognitive impairment in Parkinson disease","authors":"Panteleimon Oikonomou, Fahimeh H. Akhoundi, Nahid Olfati, Irene Litvan","doi":"10.1038/s41582-025-01163-x","DOIUrl":"10.1038/s41582-025-01163-x","url":null,"abstract":"Cognitive impairment in people with Parkinson disease (PD) imposes a substantial societal burden: PD affects over 1% of the population aged 65 years and older, and 24–31% of individuals with this condition develop dementia and another 26% present with mild cognitive impairment. Given the increasing prevalence of PD in light of an ageing population, the challenge of PD-associated cognitive impairment is likely to intensify. In this Review, we highlight the latest research advances in PD-associated cognitive impairment, emphasizing emerging mechanistic insights and new biomarkers. We outline the epidemiology and natural history of cognitive decline in PD, focusing on prodromal stages and the closely related spectrum of Lewy body dementia. We discuss key pathophysiological factors and mechanisms, including aggregation and prion-like propagation of α-synuclein; co-pathologies; synaptic dysfunction; genetics; neuroinflammation; mitochondrial dysfunction; oxidative stress; microbiome alterations; degeneration of cholinergic and monoaminergic systems; autonomic dysfunction; altered neuronal network activity; and glymphatic impairment. We consider how advances in fluid and neuroimaging biomarkers, together with preclinical disease models and pathological studies, are providing insights into these mechanisms. A deeper understanding of the multifaceted pathophysiology of PD-associated cognitive impairment will help us to explain the heterogeneity of cognitive profiles and disease progression in PD, providing a foundation for personalized disease-modifying treatments. Cognitive impairment is one of a range of non-motor symptoms that people with Parkinson disease (PD) can experience in addition to the hallmark motor symptoms of the disease. In this Review, Oikonomou et al. outline the epidemiology and natural history of cognitive decline in PD and related disorders, and discuss the key underlying pathophysiological factors and mechanisms.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 2","pages":"90-109"},"PeriodicalIF":33.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664238","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 : 2025-11-28DOI: 10.1038/s41582-025-01162-y
Guy C. Brown, Peter St George-Hyslop, Rosa C. Paolicelli, Greg Lemke
Accumulating evidence indicates that Alzheimer disease (AD) is caused by dysregulated microglial phagocytosis. The main risk factor for AD is age, and ageing reduces microglial phagocytosis of amyloid-β (Aβ) plaques, while increasing microglial phagocytosis of synapses and neurons. Most of the known genetic risk for AD can be linked to microglial phagocytosis, including ABCA1, ABI3, ACE, ADAM17, APOE, APP, BIN1, BLNK, CD2AP, CD33, CLU, CR1, CTSB, CTSH, EED, GRN, INPP5D, LILRB2, PICALM, PLCG2, PSEN1, PTK2B, SIGLEC11, SORL1, SPI1, TMEM106B and TREM2. Moreover, the only disease-modifying treatments for AD — anti-Aβ antibodies — work by increasing microglial phagocytosis of Aβ aggregates. Microglial phagocytosis of Aβ via TREM2, LRP1, CD33, TAM receptors and anti-Aβ antibodies appears to reduce AD pathology by pruning and compacting plaques, restricting subsequent tau pathology, whereas microglial phagocytosis of synapses and neurons seems detrimental in the later stages of AD, via complement, P2Y6 receptor and TREM2. However, the roles of microglial phagocytosis in AD are complex and multifaceted, and improved treatments are likely to require a deeper understanding of these roles. Growing evidence indicates important roles for microglial phagocytosis in Alzheimer disease. This Review summarizes the latest insights into the mechanisms by which microglial phagocytosis can affect Alzheimer disease pathology and how this process might be harnessed for therapeutic interventions.
{"title":"Microglial phagocytosis in Alzheimer disease","authors":"Guy C. Brown, Peter St George-Hyslop, Rosa C. Paolicelli, Greg Lemke","doi":"10.1038/s41582-025-01162-y","DOIUrl":"10.1038/s41582-025-01162-y","url":null,"abstract":"Accumulating evidence indicates that Alzheimer disease (AD) is caused by dysregulated microglial phagocytosis. The main risk factor for AD is age, and ageing reduces microglial phagocytosis of amyloid-β (Aβ) plaques, while increasing microglial phagocytosis of synapses and neurons. Most of the known genetic risk for AD can be linked to microglial phagocytosis, including ABCA1, ABI3, ACE, ADAM17, APOE, APP, BIN1, BLNK, CD2AP, CD33, CLU, CR1, CTSB, CTSH, EED, GRN, INPP5D, LILRB2, PICALM, PLCG2, PSEN1, PTK2B, SIGLEC11, SORL1, SPI1, TMEM106B and TREM2. Moreover, the only disease-modifying treatments for AD — anti-Aβ antibodies — work by increasing microglial phagocytosis of Aβ aggregates. Microglial phagocytosis of Aβ via TREM2, LRP1, CD33, TAM receptors and anti-Aβ antibodies appears to reduce AD pathology by pruning and compacting plaques, restricting subsequent tau pathology, whereas microglial phagocytosis of synapses and neurons seems detrimental in the later stages of AD, via complement, P2Y6 receptor and TREM2. However, the roles of microglial phagocytosis in AD are complex and multifaceted, and improved treatments are likely to require a deeper understanding of these roles. Growing evidence indicates important roles for microglial phagocytosis in Alzheimer disease. This Review summarizes the latest insights into the mechanisms by which microglial phagocytosis can affect Alzheimer disease pathology and how this process might be harnessed for therapeutic interventions.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 1","pages":"54-69"},"PeriodicalIF":33.1,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145611326","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 : 2025-11-27DOI: 10.1038/s41582-025-01164-w
Ruth Dobson,Karim L Kreft,Benjamin M Jacobs,J William L Brown,Alison Thomson,Richard Nicholas,Clare Walton,Parth Narendran,
Multiple sclerosis (MS) is among the most common causes of disability in the young and, despite the advent of highly effective disease-modifying therapies, remains an incurable disease. Prevention of MS before the onset of demyelination is a feasible, albeit ambitious, goal. Currently, preventive interventions with adequate evidence of efficacy are lacking, and evaluating such interventions with traditional trial designs is challenging. Additionally, the high frequency and low effect sizes of putative MS risk factors, a limited window of opportunity to intervene, and the relatively low incidence of MS in the general population make prevention studies conceptually and practically difficult. Nevertheless, studies in radiologically isolated syndrome have generated momentum within the MS prevention space, and novel trial designs offer the potential for reimagining traditional randomized controlled trials. In this Perspective, we discuss the challenges in developing and testing preventive interventions in MS and, drawing on progress in other diseases, we propose strategies and solutions. We discuss pragmatic approaches to risk stratification and illustrate the importance of considering statistical power and outcome definitions. Prevention studies require careful thought with respect to risk stratification, communication, intervention and outcomes but, given the current knowledge, the time to set up and start MS prediction and prevention studies is now.
{"title":"Towards primary prevention of multiple sclerosis.","authors":"Ruth Dobson,Karim L Kreft,Benjamin M Jacobs,J William L Brown,Alison Thomson,Richard Nicholas,Clare Walton,Parth Narendran, ","doi":"10.1038/s41582-025-01164-w","DOIUrl":"https://doi.org/10.1038/s41582-025-01164-w","url":null,"abstract":"Multiple sclerosis (MS) is among the most common causes of disability in the young and, despite the advent of highly effective disease-modifying therapies, remains an incurable disease. Prevention of MS before the onset of demyelination is a feasible, albeit ambitious, goal. Currently, preventive interventions with adequate evidence of efficacy are lacking, and evaluating such interventions with traditional trial designs is challenging. Additionally, the high frequency and low effect sizes of putative MS risk factors, a limited window of opportunity to intervene, and the relatively low incidence of MS in the general population make prevention studies conceptually and practically difficult. Nevertheless, studies in radiologically isolated syndrome have generated momentum within the MS prevention space, and novel trial designs offer the potential for reimagining traditional randomized controlled trials. In this Perspective, we discuss the challenges in developing and testing preventive interventions in MS and, drawing on progress in other diseases, we propose strategies and solutions. We discuss pragmatic approaches to risk stratification and illustrate the importance of considering statistical power and outcome definitions. Prevention studies require careful thought with respect to risk stratification, communication, intervention and outcomes but, given the current knowledge, the time to set up and start MS prediction and prevention studies is now.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"15 1","pages":""},"PeriodicalIF":38.1,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145613231","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 : 2025-11-26DOI: 10.1038/s41582-025-01161-z
Nahal Farhani, Yakdehikandage S. Costa, Marina Rozik, Karen Spruyt, Arthur S. Walters, Mark I. Boulos
Restless legs syndrome (RLS) and periodic limb movements (PLMs) are increasingly recognized as risk factors for cerebrovascular and cardiovascular diseases, particularly stroke. Conversely, stroke can precipitate or exacerbate the symptoms of RLS and PLMs. This Review explores the shared pathophysiological mechanisms linking RLS and PLMs to cerebrovascular pathology, highlighting a bidirectional relationship. We discuss mechanisms including neurotransmitter dysregulation, autonomic dysfunction, inflammation, oxidative stress, hypoxia and genomic and proteomic factors. Furthermore, we summarize emerging evidence and provide new insights on the potential clinical relevance of RLS in cerebrovascular risk assessment and management. Restless legs syndrome and periodic limb movements are increasingly recognized as risk factors for stroke and other cerebrovascular and cardiovascular diseases and vice versa. This Review explores the shared pathophysiological mechanisms that could underly this bidirectional relationship.
{"title":"Restless legs syndrome and periodic limb movements of sleep — the relationship with stroke and other cerebrovascular disease","authors":"Nahal Farhani, Yakdehikandage S. Costa, Marina Rozik, Karen Spruyt, Arthur S. Walters, Mark I. Boulos","doi":"10.1038/s41582-025-01161-z","DOIUrl":"10.1038/s41582-025-01161-z","url":null,"abstract":"Restless legs syndrome (RLS) and periodic limb movements (PLMs) are increasingly recognized as risk factors for cerebrovascular and cardiovascular diseases, particularly stroke. Conversely, stroke can precipitate or exacerbate the symptoms of RLS and PLMs. This Review explores the shared pathophysiological mechanisms linking RLS and PLMs to cerebrovascular pathology, highlighting a bidirectional relationship. We discuss mechanisms including neurotransmitter dysregulation, autonomic dysfunction, inflammation, oxidative stress, hypoxia and genomic and proteomic factors. Furthermore, we summarize emerging evidence and provide new insights on the potential clinical relevance of RLS in cerebrovascular risk assessment and management. Restless legs syndrome and periodic limb movements are increasingly recognized as risk factors for stroke and other cerebrovascular and cardiovascular diseases and vice versa. This Review explores the shared pathophysiological mechanisms that could underly this bidirectional relationship.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 1","pages":"37-53"},"PeriodicalIF":33.1,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145599317","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 : 2025-11-25DOI: 10.1038/s41582-025-01170-y
Heather Wood, Victor Rivera
Nature Reviews Neurology is interviewing individuals who are driving efforts to address disparities in neurology through a broad spectrum of diversity, equity and inclusion initiatives. We spoke with Victor Rivera from Baylor College of Medicine about his work to address disparities in multiple sclerosis care in Latin American and other populations.
{"title":"Addressing multiple sclerosis disparities in Latin American and other populations","authors":"Heather Wood, Victor Rivera","doi":"10.1038/s41582-025-01170-y","DOIUrl":"10.1038/s41582-025-01170-y","url":null,"abstract":"Nature Reviews Neurology is interviewing individuals who are driving efforts to address disparities in neurology through a broad spectrum of diversity, equity and inclusion initiatives. We spoke with Victor Rivera from Baylor College of Medicine about his work to address disparities in multiple sclerosis care in Latin American and other populations.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 1","pages":"1-2"},"PeriodicalIF":33.1,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593719","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 : 2025-11-17DOI: 10.1038/s41582-025-01160-0
Jefferson Becker, Milena Sales Pitombeira, Juan Ignacio Rojas
According to the MS International Federation, the global prevalence of multiple sclerosis (MS) is increasing, although regional variations have been reported, which could provide valuable insights into MS pathophysiology. As we highlight in this Review, the prevalence of MS in Latin America is comparatively low, possibly owing at least in part to the unique genetic and environmental characteristics of this region. Latin America has experienced centuries of admixture between Native American Indian populations and people from other parts of the world, including Europe and — to a lesser extent — Africa. Moreover, certain environmental factors in the Southern Hemisphere might contribute to this reduced MS prevalence. The McDonald criteria are considered to be a useful tool to diagnose MS in Latin America, although it is important to exclude regional diseases that can mimic MS. MS research is burgeoning in the region, and increasing numbers of Latin American patients are participating in randomized clinical trials. In addition, real-world data from national and regional MS registries are helping us to understand the distinct features of the disease in Latin America. This article reviews the epidemiology and clinical characteristics of multiple sclerosis (MS) in Latin America and how they might be influenced by genetic, environmental and socioeconomic factors that are unique to this region. The authors also describe diagnostic criteria, differential diagnosis and current approaches to MS treatment and management in Latin American countries.
{"title":"Epidemiology and characteristics of multiple sclerosis in Latin America","authors":"Jefferson Becker, Milena Sales Pitombeira, Juan Ignacio Rojas","doi":"10.1038/s41582-025-01160-0","DOIUrl":"10.1038/s41582-025-01160-0","url":null,"abstract":"According to the MS International Federation, the global prevalence of multiple sclerosis (MS) is increasing, although regional variations have been reported, which could provide valuable insights into MS pathophysiology. As we highlight in this Review, the prevalence of MS in Latin America is comparatively low, possibly owing at least in part to the unique genetic and environmental characteristics of this region. Latin America has experienced centuries of admixture between Native American Indian populations and people from other parts of the world, including Europe and — to a lesser extent — Africa. Moreover, certain environmental factors in the Southern Hemisphere might contribute to this reduced MS prevalence. The McDonald criteria are considered to be a useful tool to diagnose MS in Latin America, although it is important to exclude regional diseases that can mimic MS. MS research is burgeoning in the region, and increasing numbers of Latin American patients are participating in randomized clinical trials. In addition, real-world data from national and regional MS registries are helping us to understand the distinct features of the disease in Latin America. This article reviews the epidemiology and clinical characteristics of multiple sclerosis (MS) in Latin America and how they might be influenced by genetic, environmental and socioeconomic factors that are unique to this region. The authors also describe diagnostic criteria, differential diagnosis and current approaches to MS treatment and management in Latin American countries.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 1","pages":"22-36"},"PeriodicalIF":33.1,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145536367","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 : 2025-11-13DOI: 10.1038/s41582-025-01159-7
Jasmine Donaldson, Davina Hensman Moss, Marc Ciosi, Karen Usdin, Gabriel Balmus, Darren G. Monckton, Sarah J. Tabrizi
Expansion of simple DNA repeats causes over 45 human, predominantly neurodegenerative, inherited disorders. Huntington disease is a fatal, inherited, neurodegenerative disease caused by a CAG repeat expansion in the huntingtin gene (HTT), resulting in a toxic polyglutamine tract in the huntingtin protein. The disease leads to progressive motor, cognitive and psychiatric decline, primarily resulting from loss of medium spiny neurons in the striatum. Although Huntington disease has long been viewed as a consequence of age-dependent toxicity from mutant huntingtin, genome-wide association studies have identified genetic modifiers, mostly DNA repair genes, that significantly influence disease onset and progression. These findings point to somatic CAG repeat expansions in affected tissues as a key pathological mechanism. This emerging paradigm suggests that disease progression is not solely protein-driven but also shaped at the DNA level, a mechanism that is shared among other repeat expansion disorders. Therapeutically, this discovery opens new opportunities: interventions to limit somatic repeat expansion might be effective across multiple repeat expansion diseases and, when combined with disease-specific approaches, such as huntingtin lowering in Huntington disease, might offer more effective and longer-lasting clinical benefits than either strategy in isolation. This approach also poses challenges, determining the optimal point for therapeutic intervention and how best to establish phenotypic improvement in clinical trials when the target tissue is the brain. Genome-wide association studies have identified genetic modifiers, mostly DNA repair genes, that significantly influence the onset and progression of Huntington disease, pointing to somatic CAG repeat expansions as a key pathological driver. Here, Tabrizi and colleagues review the evidence for this paradigm and discuss the potential for therapeutic interventions.
{"title":"Huntington disease: somatic expansion, pathobiology and therapeutics","authors":"Jasmine Donaldson, Davina Hensman Moss, Marc Ciosi, Karen Usdin, Gabriel Balmus, Darren G. Monckton, Sarah J. Tabrizi","doi":"10.1038/s41582-025-01159-7","DOIUrl":"10.1038/s41582-025-01159-7","url":null,"abstract":"Expansion of simple DNA repeats causes over 45 human, predominantly neurodegenerative, inherited disorders. Huntington disease is a fatal, inherited, neurodegenerative disease caused by a CAG repeat expansion in the huntingtin gene (HTT), resulting in a toxic polyglutamine tract in the huntingtin protein. The disease leads to progressive motor, cognitive and psychiatric decline, primarily resulting from loss of medium spiny neurons in the striatum. Although Huntington disease has long been viewed as a consequence of age-dependent toxicity from mutant huntingtin, genome-wide association studies have identified genetic modifiers, mostly DNA repair genes, that significantly influence disease onset and progression. These findings point to somatic CAG repeat expansions in affected tissues as a key pathological mechanism. This emerging paradigm suggests that disease progression is not solely protein-driven but also shaped at the DNA level, a mechanism that is shared among other repeat expansion disorders. Therapeutically, this discovery opens new opportunities: interventions to limit somatic repeat expansion might be effective across multiple repeat expansion diseases and, when combined with disease-specific approaches, such as huntingtin lowering in Huntington disease, might offer more effective and longer-lasting clinical benefits than either strategy in isolation. This approach also poses challenges, determining the optimal point for therapeutic intervention and how best to establish phenotypic improvement in clinical trials when the target tissue is the brain. Genome-wide association studies have identified genetic modifiers, mostly DNA repair genes, that significantly influence the onset and progression of Huntington disease, pointing to somatic CAG repeat expansions as a key pathological driver. Here, Tabrizi and colleagues review the evidence for this paradigm and discuss the potential for therapeutic interventions.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"22 1","pages":"5-21"},"PeriodicalIF":33.1,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145509072","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 : 2025-11-11DOI: 10.1038/s41582-025-01167-7
Ian Fyfe
PET imaging of synaptic vesicle protein 2A could enable visualization of grey matter pathology in multiple sclerosis, new work has shown.
新的研究表明，突触囊泡蛋白2A的PET成像可以使多发性硬化症的灰质病理可视化。
{"title":"PET imaging of progression in multiple sclerosis","authors":"Ian Fyfe","doi":"10.1038/s41582-025-01167-7","DOIUrl":"10.1038/s41582-025-01167-7","url":null,"abstract":"PET imaging of synaptic vesicle protein 2A could enable visualization of grey matter pathology in multiple sclerosis, new work has shown.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"668-668"},"PeriodicalIF":33.1,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145491687","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 : 2025-11-11DOI: 10.1038/s41582-025-01169-5
Lisa Kiani
Lipids derived from extracellular vesicles in adipose tissue from people with obesity can promote amyloid-β aggregation, according to new research.
根据一项新的研究，来自肥胖人群脂肪组织细胞外囊泡的脂质可以促进淀粉样蛋白-β聚集。
{"title":"Obesity-associated extracellular vesicle lipids modulate amyloid-β aggregation","authors":"Lisa Kiani","doi":"10.1038/s41582-025-01169-5","DOIUrl":"10.1038/s41582-025-01169-5","url":null,"abstract":"Lipids derived from extracellular vesicles in adipose tissue from people with obesity can promote amyloid-β aggregation, according to new research.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"667-667"},"PeriodicalIF":33.1,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145491710","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 : 2025-11-11DOI: 10.1038/s41582-025-01165-9
Ian Fyfe
The C9orf72 hexanucleotide expansion that causes amyotrophic lateral sclerosis (ALS) compromises microglial function, new research has shown.
新的研究表明，引起肌萎缩性侧索硬化症（ALS）的C9orf72六核苷酸扩增会损害小胶质细胞的功能。
{"title":"Microglia response altered by ALS mutation","authors":"Ian Fyfe","doi":"10.1038/s41582-025-01165-9","DOIUrl":"10.1038/s41582-025-01165-9","url":null,"abstract":"The C9orf72 hexanucleotide expansion that causes amyotrophic lateral sclerosis (ALS) compromises microglial function, new research has shown.","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":"21 12","pages":"667-667"},"PeriodicalIF":33.1,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145491690","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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