Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00363-1
Sonja W Scholz, Njideka U Okubadejo, Priya Prakash, Shane A Liddelow, Mina Ryten, Glenda M Halliday
Lewy body dementia is a heterogeneous disease that is underdiagnosed and poorly understood. Pathologically, Lewy body dementia is characterised by the accumulation of intraneuronal aggregates of misfolded α-synuclein, known as Lewy bodies and Lewy neurites. The genetic architecture of Lewy body dementia is complex, involving both common genetic variants with small risk effects and rare genetic variants with large effects. Alzheimer's disease pathology frequently coexists with Lewy body pathology and influences the clinical presentation. A deeper understanding of the pathophysiological pathways, including mitochondrial dysfunction, lysosomal dysfunction, and neuroinflammation, can enhance disease modelling, and this knowledge will ultimately facilitate the development of therapeutic interventions. The biological relationships that Lewy body dementia shares with other neurodegenerative and psychiatric disorders might also be crucial for the development of therapeutic strategies.
{"title":"Advances in the genetics and pathology of Lewy body dementia","authors":"Sonja W Scholz, Njideka U Okubadejo, Priya Prakash, Shane A Liddelow, Mina Ryten, Glenda M Halliday","doi":"10.1016/s1474-4422(25)00363-1","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00363-1","url":null,"abstract":"Lewy body dementia is a heterogeneous disease that is underdiagnosed and poorly understood. Pathologically, Lewy body dementia is characterised by the accumulation of intraneuronal aggregates of misfolded α-synuclein, known as Lewy bodies and Lewy neurites. The genetic architecture of Lewy body dementia is complex, involving both common genetic variants with small risk effects and rare genetic variants with large effects. Alzheimer's disease pathology frequently coexists with Lewy body pathology and influences the clinical presentation. A deeper understanding of the pathophysiological pathways, including mitochondrial dysfunction, lysosomal dysfunction, and neuroinflammation, can enhance disease modelling, and this knowledge will ultimately facilitate the development of therapeutic interventions. The biological relationships that Lewy body dementia shares with other neurodegenerative and psychiatric disorders might also be crucial for the development of therapeutic strategies.","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"181 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00393-x
Manley GT, Dams-O’Connor K, Alosco ML, et al. A new characterisation of acute traumatic brain injury: the NIH-NINDS TBI Classification and Nomenclature Initiative. Lancet Neurology 2025; 24: 512–23—In this Policy Review, Rachel Sayko Adam's name was listed incorrectly in the appendix. This correction has been made to the online version as of Nov 12, 2025.
{"title":"Correction to Lancet Neurol 2025; 24: 512–23","authors":"","doi":"10.1016/s1474-4422(25)00393-x","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00393-x","url":null,"abstract":"<em>Manley GT, Dams-O’Connor K, Alosco ML, et al. A new characterisation of acute traumatic brain injury: the NIH-NINDS TBI Classification and Nomenclature Initiative.</em> Lancet Neurology <em>2025; <strong>24:</strong> 512–23</em>—In this Policy Review, Rachel Sayko Adam's name was listed incorrectly in the appendix. This correction has been made to the online version as of Nov 12, 2025.","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00381-3
Raúl Martínez-Fernández, Steffen Paschen, Günther Deuschl, José A Obeso
No Abstract
没有抽象的
{"title":"Focused ultrasound pallidothalamic tractotomy for Parkinson's disease: the field is moving fast","authors":"Raúl Martínez-Fernández, Steffen Paschen, Günther Deuschl, José A Obeso","doi":"10.1016/s1474-4422(25)00381-3","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00381-3","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"115 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00384-9
Nadia Soliman, Xavier Moisset, Nadine Attal, Nanna B Finnerup, Simon Haroutounian
No Abstract
没有抽象的
{"title":"Caution on the use of α2δ-ligands in neuropathic pain – Authors' reply","authors":"Nadia Soliman, Xavier Moisset, Nadine Attal, Nanna B Finnerup, Simon Haroutounian","doi":"10.1016/s1474-4422(25)00384-9","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00384-9","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"53 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00395-3
Blauwendraat C, Morris HR, Keuren-Jensen KV, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention. Lancet Neurol 2025; 24: 969–75—In this Personal View, figures 1 and 2 were transposed. This correction has been made to the online version as of Nov 12, 2025.
{"title":"Correction to Lancet Neurol 2025; 24: 969–75","authors":"","doi":"10.1016/s1474-4422(25)00395-3","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00395-3","url":null,"abstract":"<em>Blauwendraat C, Morris HR, Keuren-Jensen KV, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention.</em> Lancet Neurol <em>2025; <strong>24:</strong> 969–75</em>—In this Personal View, figures 1 and 2 were transposed. This correction has been made to the online version as of Nov 12, 2025.","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-13DOI: 10.1016/s1474-4422(25)00314-x
Angeliki Zarkali, Michael Bartl, Nick C Fox, Louis C S Tan, Brit Mollenhauer, Rimona S Weil
Dementia with Lewy bodies is characterised clinically by visual hallucinations, fluctuating cognitive function, parkinsonism, and rapid eye movement sleep behaviour disorder, and can cause more frailty than other dementias. The disease is heterogeneous in presentation and progression, and misdiagnoses are common. In people with dementia with Lewy bodies, other brain copathologies are frequent, limiting the usefulness of some diagnostic biomarkers. This heterogeneity, together with the scarcity of diagnostic and prognostic biomarkers, has hindered the implementation of therapeutic trials. However, novel neuroimaging techniques have emerged with high sensitivity to brain tissue composition and microstructure. Fluid biomarkers are being developed to detect very low concentrations of neuropathological proteins. These biomarkers could soon be adopted in clinical practice and incorporated as outcome measures in clinical trials. These advances will pave the way for early diagnosis, disease monitoring, and prognosis, and will facilitate the implementation of disease-modifying trials.
{"title":"Diagnostic and other biomarkers of dementia with Lewy bodies: from research to clinical settings","authors":"Angeliki Zarkali, Michael Bartl, Nick C Fox, Louis C S Tan, Brit Mollenhauer, Rimona S Weil","doi":"10.1016/s1474-4422(25)00314-x","DOIUrl":"https://doi.org/10.1016/s1474-4422(25)00314-x","url":null,"abstract":"Dementia with Lewy bodies is characterised clinically by visual hallucinations, fluctuating cognitive function, parkinsonism, and rapid eye movement sleep behaviour disorder, and can cause more frailty than other dementias. The disease is heterogeneous in presentation and progression, and misdiagnoses are common. In people with dementia with Lewy bodies, other brain copathologies are frequent, limiting the usefulness of some diagnostic biomarkers. This heterogeneity, together with the scarcity of diagnostic and prognostic biomarkers, has hindered the implementation of therapeutic trials. However, novel neuroimaging techniques have emerged with high sensitivity to brain tissue composition and microstructure. Fluid biomarkers are being developed to detect very low concentrations of neuropathological proteins. These biomarkers could soon be adopted in clinical practice and incorporated as outcome measures in clinical trials. These advances will pave the way for early diagnosis, disease monitoring, and prognosis, and will facilitate the implementation of disease-modifying trials.","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"115 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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