Pub Date : 2024-11-20DOI: 10.1016/s1474-4422(24)00480-0
Jules Morgan
No Abstract
无摘要
{"title":"Creative neurorehabilitation: the art of intervention","authors":"Jules Morgan","doi":"10.1016/s1474-4422(24)00480-0","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00480-0","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"128 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678227","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00452-6
Monfrini E, Minardi R, Valzania F, Calandra-Buonaura G, Mandich P, Di Fonzo A. RAB32 mutation in Parkinson's disease. Lancet Neurol 2024; 23: 961–62—The appendix has been updated to include a list of ParkNet Study Group members who were involved in this project. This correction has been made as of Nov 20, 2024.
{"title":"Correction to Lancet Neurol 2024; 23: 961–62","authors":"","doi":"10.1016/s1474-4422(24)00452-6","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00452-6","url":null,"abstract":"<em>Monfrini E, Minardi R, Valzania F, Calandra-Buonaura G, Mandich P, Di Fonzo A.</em> RAB32 <em>mutation in Parkinson's disease. Lancet Neurol 2024; <strong>23:</strong> 961–62</em>—The appendix has been updated to include a list of ParkNet Study Group members who were involved in this project. This correction has been made as of Nov 20, 2024.","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678240","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00428-9
James A Wiseman, Glenda M Halliday, Birger Victor Dieriks
No Abstract
无摘要
{"title":"A new seed amplification assay to diagnose multiple system atrophy","authors":"James A Wiseman, Glenda M Halliday, Birger Victor Dieriks","doi":"10.1016/s1474-4422(24)00428-9","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00428-9","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678235","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00425-3
Kevin N Sheth, Gregory W Albers, Jeffrey L Saver, Bruce C V Campbell, Bradley J Molyneaux, H E Hinson, Charlotte Cordonnier, Thorsten Steiner, Kazunori Toyoda, Max Wintermark, Ross Littauer, Jessica Collins, Nisha Lucas, Raul G Nogueira, J Marc Simard, Michael Wald, Kate Dawson, W Taylor Kimberly
<h3>Background</h3>No treatment is available to prevent brain oedema, which can occur after a large hemispheric infarction. Glibenclamide has previously been shown to improve functional outcome and reduce neurological or oedema-related death in patients younger than 70 years who were at risk of brain oedema after an acute ischaemic stroke. We aimed to assess whether intravenous glibenclamide could improve functional outcome at 90 days in patients with large hemispheric infarction.<h3>Methods</h3>CHARM was a phase 3, double-blind, placebo-controlled, randomised trial conducted across 143 acute stroke centres in 21 countries. We included patients aged 18–85 years with a large stroke, defined either by an Alberta Stroke Program Early CT Score (ASPECTS) of 1–5 or by an ischaemic core lesion volume of 80–300 mL on CT perfusion or MRI diffusion-weighted imaging. Patients were randomly assigned in a 1:1 ratio to either intravenous glibenclamide (8·6 mg over 72 h) or placebo. The study drug was started within 10 h of stroke onset. The primary efficacy outcome was the shift in the distribution of scores on the modified Rankin Scale at day 90, as a measure of functional outcome. The primary efficacy outcome was analysed in a modified intention-to-treat population, which included all randomly assigned patients aged 18–70 years. The safety population comprised all randomly assigned patients who received a dose. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span> (<span><span>NCT02864953</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>). The trial was stopped early by the sponsor for strategic and operational reasons (slow enrolment because of COVID-19), before any unblinding or knowledge of the trial results.<h3>Findings</h3>Between Aug 29, 2018, and May 23, 2023, 535 patients were enrolled and randomly assigned, of whom 518 received a dose (safety population) and 431 were aged 18–70 years and comprised the modified intention-to-treat population (217 were assigned glibenclamide and 214 placebo). The mean age of patients was 58·7 (SD 9·0) years in the placebo group and 58·0 (9·5) years in the glibenclamide group; the median US National Institutes of Health Stroke Scale (NIHSS) score was 19 (IQR 16–23) in the placebo group and 19 (IQR 16–22) in the glibenclamide group; and the mean time from stroke onset to study drug start was 8·9 h (SD 2·1) in the placebo group and 9·2 h (2·1) in the glibenclamide group. Intravenous glibenclamide was not associated with a favourable shift in the modified Rankin scale at 90 days (common odds ratio [OR] 1·17 [95% CI 0·80–1·71], p=0·42). 90-day mortal
{"title":"Intravenous glibenclamide for cerebral oedema after large hemispheric stroke (CHARM): a phase 3, double-blind, placebo-controlled, randomised trial","authors":"Kevin N Sheth, Gregory W Albers, Jeffrey L Saver, Bruce C V Campbell, Bradley J Molyneaux, H E Hinson, Charlotte Cordonnier, Thorsten Steiner, Kazunori Toyoda, Max Wintermark, Ross Littauer, Jessica Collins, Nisha Lucas, Raul G Nogueira, J Marc Simard, Michael Wald, Kate Dawson, W Taylor Kimberly","doi":"10.1016/s1474-4422(24)00425-3","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00425-3","url":null,"abstract":"<h3>Background</h3>No treatment is available to prevent brain oedema, which can occur after a large hemispheric infarction. Glibenclamide has previously been shown to improve functional outcome and reduce neurological or oedema-related death in patients younger than 70 years who were at risk of brain oedema after an acute ischaemic stroke. We aimed to assess whether intravenous glibenclamide could improve functional outcome at 90 days in patients with large hemispheric infarction.<h3>Methods</h3>CHARM was a phase 3, double-blind, placebo-controlled, randomised trial conducted across 143 acute stroke centres in 21 countries. We included patients aged 18–85 years with a large stroke, defined either by an Alberta Stroke Program Early CT Score (ASPECTS) of 1–5 or by an ischaemic core lesion volume of 80–300 mL on CT perfusion or MRI diffusion-weighted imaging. Patients were randomly assigned in a 1:1 ratio to either intravenous glibenclamide (8·6 mg over 72 h) or placebo. The study drug was started within 10 h of stroke onset. The primary efficacy outcome was the shift in the distribution of scores on the modified Rankin Scale at day 90, as a measure of functional outcome. The primary efficacy outcome was analysed in a modified intention-to-treat population, which included all randomly assigned patients aged 18–70 years. The safety population comprised all randomly assigned patients who received a dose. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> (<span><span>NCT02864953</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>). The trial was stopped early by the sponsor for strategic and operational reasons (slow enrolment because of COVID-19), before any unblinding or knowledge of the trial results.<h3>Findings</h3>Between Aug 29, 2018, and May 23, 2023, 535 patients were enrolled and randomly assigned, of whom 518 received a dose (safety population) and 431 were aged 18–70 years and comprised the modified intention-to-treat population (217 were assigned glibenclamide and 214 placebo). The mean age of patients was 58·7 (SD 9·0) years in the placebo group and 58·0 (9·5) years in the glibenclamide group; the median US National Institutes of Health Stroke Scale (NIHSS) score was 19 (IQR 16–23) in the placebo group and 19 (IQR 16–22) in the glibenclamide group; and the mean time from stroke onset to study drug start was 8·9 h (SD 2·1) in the placebo group and 9·2 h (2·1) in the glibenclamide group. Intravenous glibenclamide was not associated with a favourable shift in the modified Rankin scale at 90 days (common odds ratio [OR] 1·17 [95% CI 0·80–1·71], p=0·42). 90-day mortal","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678251","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00426-5
Emily K Schworer, Matthew D Zammit, Jiebiao Wang, Benjamin L Handen, Tobey Betthauser, Charles M Laymon, Dana L Tudorascu, Annie D Cohen, Shahid H Zaman, Beau M Ances, Mark Mapstone, Elizabeth Head, Bradley T Christian, Sigan L Hartley
<h3>Background</h3>Adults with Down syndrome are at risk for Alzheimer's disease. Natural history cohort studies have characterised the progression of Alzheimer's disease biomarkers in people with Down syndrome, with a focus on amyloid β-PET and tau-PET. In this study, we aimed to leverage these well characterised imaging biomarkers in a large cohort of individuals with Down syndrome, to examine the timeline to symptomatic Alzheimer's disease based on estimated years since the detection on PET of amyloid β-positivity, referred to here as amyloid age, and in relation to tau burden as assessed by PET.<h3>Methods</h3>In this prospective, longitudinal, observational cohort study, data were collected at four university research sites in the UK and USA as part of the Alzheimer's Biomarker Consortium–Down Syndrome (ABC–DS) study. Eligible participants were aged 25 years or older with Down syndrome, had a mental age of at least 3 years (based on a standardised intelligence quotient test), and had trisomy 21 (full, mosaic, or translocation) confirmed through karyotyping. Participants were assessed twice between 2017 and 2022, with approximately 32 months between visits. Participants had amyloid-PET and tau-PET scans, and underwent cognitive assessment with the modified Cued Recall Test (mCRT) and the Down Syndrome Mental Status Examination (DSMSE) to assess cognitive functioning. Study partners completed the National Task Group-Early Detection Screen for Dementia (NTG-EDSD). Generalised linear models were used to assess the association between amyloid age (whereby 0 years equated to 18 centiloids) and mCRT, DSMSE, NTG-EDSD, and tau PET at baseline and the 32-month follow-up. Broken stick regression was used to identify the amyloid age that corresponded to decreases in cognitive performance and increases in tau PET after the onset of amyloid β positivity.<h3>Findings</h3>167 adults with Down syndrome, of whom 92 had longitudinal data, were included in our analyses. Generalised linear regressions showed significant quadratic associations between amyloid age and cognitive performance and cubic associations between amyloid age and tau, both at baseline and at the 32-month follow-up. Using broken stick regression models, differences in mCRT total scores were detected beginning 2·7 years (95% credible interval [CrI] 0·2 to 5·4; equating to 29·8 centiloids) after the onset of amyloid β positivity in cross-sectional models. Based on cross-sectional data, increases in tau deposition started a mean of 2·7–6·1 years (equating to 29·8–47·9 centiloids) after the onset of amyloid β positivity. Mild cognitive impairment was observed at a mean amyloid age of 7·4 years (SD 6·6; equating to 56·8 centiloids) and dementia was observed at a mean amyloid age of 12·7 years (5·6; equating to 97·4 centiloids).<h3>Interpretation</h3>There is a short timeline to initial cognitive decline and dementia from onset of amyloid β positivity and tau deposition in people with Down syndrome
背景唐氏综合征成人有罹患阿尔茨海默病的风险。自然史队列研究描述了唐氏综合征患者阿尔茨海默病生物标志物的进展，重点是淀粉样蛋白 β-PET 和 tau-PET。在这项研究中，我们的目标是在一个大型唐氏综合征患者队列中利用这些特征明确的成像生物标志物，根据 PET 检测到淀粉样β阳性后的估计年限（此处称为淀粉样年龄），并结合 PET 评估的 tau 负担，研究从出现症状到阿尔茨海默病的时间轴。方法在这项前瞻性、纵向、观察性队列研究中，作为阿尔茨海默氏症生物标志物联盟-唐氏综合征（ABC-DS）研究的一部分，在英国和美国的四所大学研究机构收集了数据。符合条件的参与者年龄在25岁或25岁以上，患有唐氏综合征，心智年龄至少为3岁（基于标准化智商测试），并通过核型检查确认患有21三体综合征（全合、镶嵌或易位）。参与者在 2017 年至 2022 年期间接受了两次评估，两次评估之间相隔约 32 个月。参与者接受了淀粉样蛋白-PET和tau-PET扫描，并通过改良诱导回忆测试（mCRT）和唐氏综合征精神状态检查（DSMSE）进行了认知评估，以评估认知功能。研究伙伴完成了国家工作组-痴呆症早期检测筛查（NTG-EDSD）。采用广义线性模型评估基线和32个月随访时淀粉样蛋白年龄（0岁相当于18 centiloids）与mCRT、DSMSE、NTG-EDS和tau PET之间的关系。我们使用断棒回归法来确定淀粉样β阳性出现后，认知能力下降和tau PET增加所对应的淀粉样年龄。广义线性回归结果显示，在基线和32个月的随访中，淀粉样蛋白年龄与认知能力之间存在明显的二次方关系，而淀粉样蛋白年龄与tau之间存在明显的三次方关系。使用断棒回归模型，在横断面模型中，淀粉样β阳性开始后2-7年（95%可信区间[CrI] 0-2至5-4；相当于29-8厘洛），mCRT总分出现差异。根据横断面数据，tau沉积的增加平均始于淀粉样β阳性出现后的2-7-6-1年（相当于29-8-47-9厘洛）。唐氏综合征患者从开始出现淀粉样β阳性和tau沉积到认知能力下降和痴呆的时间很短。这一新确立的基于淀粉样蛋白年龄（或等效厘泊值）的时间线对临床实践和阿尔茨海默病临床试验的设计非常重要，它避免了基于年代年龄的时间线的局限性。
{"title":"Timeline to symptomatic Alzheimer's disease in people with Down syndrome as assessed by amyloid-PET and tau-PET: a longitudinal cohort study","authors":"Emily K Schworer, Matthew D Zammit, Jiebiao Wang, Benjamin L Handen, Tobey Betthauser, Charles M Laymon, Dana L Tudorascu, Annie D Cohen, Shahid H Zaman, Beau M Ances, Mark Mapstone, Elizabeth Head, Bradley T Christian, Sigan L Hartley","doi":"10.1016/s1474-4422(24)00426-5","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00426-5","url":null,"abstract":"<h3>Background</h3>Adults with Down syndrome are at risk for Alzheimer's disease. Natural history cohort studies have characterised the progression of Alzheimer's disease biomarkers in people with Down syndrome, with a focus on amyloid β-PET and tau-PET. In this study, we aimed to leverage these well characterised imaging biomarkers in a large cohort of individuals with Down syndrome, to examine the timeline to symptomatic Alzheimer's disease based on estimated years since the detection on PET of amyloid β-positivity, referred to here as amyloid age, and in relation to tau burden as assessed by PET.<h3>Methods</h3>In this prospective, longitudinal, observational cohort study, data were collected at four university research sites in the UK and USA as part of the Alzheimer's Biomarker Consortium–Down Syndrome (ABC–DS) study. Eligible participants were aged 25 years or older with Down syndrome, had a mental age of at least 3 years (based on a standardised intelligence quotient test), and had trisomy 21 (full, mosaic, or translocation) confirmed through karyotyping. Participants were assessed twice between 2017 and 2022, with approximately 32 months between visits. Participants had amyloid-PET and tau-PET scans, and underwent cognitive assessment with the modified Cued Recall Test (mCRT) and the Down Syndrome Mental Status Examination (DSMSE) to assess cognitive functioning. Study partners completed the National Task Group-Early Detection Screen for Dementia (NTG-EDSD). Generalised linear models were used to assess the association between amyloid age (whereby 0 years equated to 18 centiloids) and mCRT, DSMSE, NTG-EDSD, and tau PET at baseline and the 32-month follow-up. Broken stick regression was used to identify the amyloid age that corresponded to decreases in cognitive performance and increases in tau PET after the onset of amyloid β positivity.<h3>Findings</h3>167 adults with Down syndrome, of whom 92 had longitudinal data, were included in our analyses. Generalised linear regressions showed significant quadratic associations between amyloid age and cognitive performance and cubic associations between amyloid age and tau, both at baseline and at the 32-month follow-up. Using broken stick regression models, differences in mCRT total scores were detected beginning 2·7 years (95% credible interval [CrI] 0·2 to 5·4; equating to 29·8 centiloids) after the onset of amyloid β positivity in cross-sectional models. Based on cross-sectional data, increases in tau deposition started a mean of 2·7–6·1 years (equating to 29·8–47·9 centiloids) after the onset of amyloid β positivity. Mild cognitive impairment was observed at a mean amyloid age of 7·4 years (SD 6·6; equating to 56·8 centiloids) and dementia was observed at a mean amyloid age of 12·7 years (5·6; equating to 97·4 centiloids).<h3>Interpretation</h3>There is a short timeline to initial cognitive decline and dementia from onset of amyloid β positivity and tau deposition in people with Down syndrome","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678313","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00444-7
Mario Fernando Prieto Peres
No Abstract
无摘要
{"title":"PACAP pathway: a new frontier in migraine prevention","authors":"Mario Fernando Prieto Peres","doi":"10.1016/s1474-4422(24)00444-7","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00444-7","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678234","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 : 2024-11-20DOI: 10.1016/s1474-4422(24)00453-8
Marco De Ambrogi
No Abstract
无摘要
{"title":"The woman who was not there","authors":"Marco De Ambrogi","doi":"10.1016/s1474-4422(24)00453-8","DOIUrl":"https://doi.org/10.1016/s1474-4422(24)00453-8","url":null,"abstract":"No Abstract","PeriodicalId":22676,"journal":{"name":"The Lancet Neurology","volume":"71 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678244","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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