{"title":"脑卒中后淀粉样蛋白沉积的患病率与认知结果:IDEA3 研究","authors":"Olivier Godefroy , Mélanie Barbay , Jeanne Martin , Trevor Shields , Chantal Lamy , Audrey Courselle-Arnoux , Sandrine Canaple , Claire Leclercq , Martine Roussel , Marc-Etienne Meyer , Etienne Marchal , Frank A. Wollenweber","doi":"10.1016/j.cccb.2024.100279","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p>The contribution of associated Alzheimer disease to poststroke cognitive impairment has been suggested on clinical grounds. However, the few published studies using amyloid PET have provided a widely ranging prevalence and a questionable relationship with cognitive status.</p><p>The main objective of the study was to determine the prevalence of amyloid PET positivity among poststroke patients with at least one impaired cognitive score. The secondary objectives were to determine the association between clinical, cognitive, and imaging characteristics at baseline with amyloid status.</p></div><div><h3>Methods</h3><p>The IDEA3 cohort included 91 stroke patients (cerebral infarct: 89%; hemorrhage: 11%). They were assessed at 808 ± 589 days poststroke with a cognitive battery, MRI, and florbetapir PET. Clinical, cognitive, and imaging characteristics at baseline were compared according to amyloid status.</p></div><div><h3>Results</h3><p>Amyloid PET was positive for 14 patients, corresponding to a prevalence of 15.4% (95%CI: 7.97-22.8). Amyloid-positive patients were older (p = 0.0001), did not differ according to the cause of stroke, except for a tendency towards a higher frequency of cerebral amyloid angiopathy in the hemorrhagic subgroup (p = 0.06). Their cognitive performance was lower on both the cognitive screening test (p = 0.023) and battery (p = 0.02), without a specific profile.</p></div><div><h3>Discussion</h3><p>This study supports the mild prevalence of amyloid burden and shows that it contributes to poststroke cognitive impairment.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100279"},"PeriodicalIF":1.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000801/pdfft?md5=ae56a9886e08a168bd278fe74214d0bb&pid=1-s2.0-S2666245024000801-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Prevalence of Amyloid Cerebral Deposits and Cognitive Outcome After Stroke: The IDEA3 Study\",\"authors\":\"Olivier Godefroy , Mélanie Barbay , Jeanne Martin , Trevor Shields , Chantal Lamy , Audrey Courselle-Arnoux , Sandrine Canaple , Claire Leclercq , Martine Roussel , Marc-Etienne Meyer , Etienne Marchal , Frank A. 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Clinical, cognitive, and imaging characteristics at baseline were compared according to amyloid status.</p></div><div><h3>Results</h3><p>Amyloid PET was positive for 14 patients, corresponding to a prevalence of 15.4% (95%CI: 7.97-22.8). Amyloid-positive patients were older (p = 0.0001), did not differ according to the cause of stroke, except for a tendency towards a higher frequency of cerebral amyloid angiopathy in the hemorrhagic subgroup (p = 0.06). Their cognitive performance was lower on both the cognitive screening test (p = 0.023) and battery (p = 0.02), without a specific profile.</p></div><div><h3>Discussion</h3><p>This study supports the mild prevalence of amyloid burden and shows that it contributes to poststroke cognitive impairment.</p></div>\",\"PeriodicalId\":72549,\"journal\":{\"name\":\"Cerebral circulation - cognition and behavior\",\"volume\":\"6 \",\"pages\":\"Article 100279\"},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2666245024000801/pdfft?md5=ae56a9886e08a168bd278fe74214d0bb&pid=1-s2.0-S2666245024000801-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cerebral circulation - cognition and behavior\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2666245024000801\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cerebral circulation - cognition and behavior","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666245024000801","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
摘要
导言:临床研究表明,阿尔茨海默病是脑卒中后认知障碍的原因之一。本研究的主要目的是确定至少有一项认知功能受损的卒中后患者的淀粉样蛋白 PET 阳性率。次要目标是确定基线时的临床、认知和成像特征与淀粉样蛋白状态之间的关联。方法IDEA3队列包括91名脑卒中患者(脑梗塞:89%;出血:11%)。他们在中风后 808 ± 589 天时接受了认知测试、核磁共振成像和氟贝特哌啶 PET 评估。结果 14 名患者的淀粉样蛋白 PET 呈阳性,患病率为 15.4%(95%CI:7.97-22.8)。淀粉样蛋白阳性患者年龄较大(p = 0.0001),除了出血性亚组中脑淀粉样蛋白血管病变的发病率较高外(p = 0.06),其他患者的发病原因没有差异。他们的认知能力在认知筛选测试(p = 0.023)和电池测试(p = 0.02)中都较低,但没有特定的特征。
Prevalence of Amyloid Cerebral Deposits and Cognitive Outcome After Stroke: The IDEA3 Study
Introduction
The contribution of associated Alzheimer disease to poststroke cognitive impairment has been suggested on clinical grounds. However, the few published studies using amyloid PET have provided a widely ranging prevalence and a questionable relationship with cognitive status.
The main objective of the study was to determine the prevalence of amyloid PET positivity among poststroke patients with at least one impaired cognitive score. The secondary objectives were to determine the association between clinical, cognitive, and imaging characteristics at baseline with amyloid status.
Methods
The IDEA3 cohort included 91 stroke patients (cerebral infarct: 89%; hemorrhage: 11%). They were assessed at 808 ± 589 days poststroke with a cognitive battery, MRI, and florbetapir PET. Clinical, cognitive, and imaging characteristics at baseline were compared according to amyloid status.
Results
Amyloid PET was positive for 14 patients, corresponding to a prevalence of 15.4% (95%CI: 7.97-22.8). Amyloid-positive patients were older (p = 0.0001), did not differ according to the cause of stroke, except for a tendency towards a higher frequency of cerebral amyloid angiopathy in the hemorrhagic subgroup (p = 0.06). Their cognitive performance was lower on both the cognitive screening test (p = 0.023) and battery (p = 0.02), without a specific profile.
Discussion
This study supports the mild prevalence of amyloid burden and shows that it contributes to poststroke cognitive impairment.