Personalized modeling of Alzheimer's disease progression estimates neurodegeneration severity from EEG recordings

L. G. Amato, A. A. Vergani, M. Lassi, C. Fabbiani, S. Mazzeo, R. Burali, B. Nacmias, S. Sorbi, R. Mannella, A. Grippo, V. Bessi, A. Mazzoni
{"title":"Personalized modeling of Alzheimer's disease progression estimates neurodegeneration severity from EEG recordings","authors":"L. G. Amato, A. A. Vergani, M. Lassi, C. Fabbiani, S. Mazzeo, R. Burali, B. Nacmias, S. Sorbi, R. Mannella, A. Grippo, V. Bessi, A. Mazzoni","doi":"10.1002/dad2.12526","DOIUrl":null,"url":null,"abstract":"Abstract INTRODUCTION Early identification of Alzheimer's disease (AD) is necessary for a timely onset of therapeutic care. However, cortical structural alterations associated with AD are difficult to discern. METHODS We developed a cortical model of AD‐related neurodegeneration accounting for slowing of local dynamics and global connectivity degradation. In a monocentric study we collected electroencephalography (EEG) recordings at rest from participants in healthy (HC, n = 17), subjective cognitive decline (SCD, n = 58), and mild cognitive impairment (MCI, n = 44) conditions. For each patient, we estimated neurodegeneration model parameters based on individual EEG recordings. RESULTS Our model outperformed standard EEG analysis not only in discriminating between HC and MCI conditions (F1 score 0.95 vs 0.75) but also in identifying SCD patients with biological hallmarks of AD in the cerebrospinal fluid (recall 0.87 vs 0.50). DISCUSSION Personalized models could (1) support classification of MCI, (2) assess the presence of AD pathology, and (3) estimate the risk of cognitive decline progression, based only on economical and non‐invasive EEG recordings. Highlights Personalized cortical model estimating structural alterations from EEG recordings. Discrimination of Mild Cognitive Impairment (MCI) and Healthy (HC) subjects (95%) Prediction of biological markers of Alzheimer's in Subjective Decline (SCD) Subjects (87%) Transition correctly predicted for 3/3 subjects that converted from SCD to MCI after 1y","PeriodicalId":516929,"journal":{"name":"Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring","volume":"310 2","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/dad2.12526","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Abstract INTRODUCTION Early identification of Alzheimer's disease (AD) is necessary for a timely onset of therapeutic care. However, cortical structural alterations associated with AD are difficult to discern. METHODS We developed a cortical model of AD‐related neurodegeneration accounting for slowing of local dynamics and global connectivity degradation. In a monocentric study we collected electroencephalography (EEG) recordings at rest from participants in healthy (HC, n = 17), subjective cognitive decline (SCD, n = 58), and mild cognitive impairment (MCI, n = 44) conditions. For each patient, we estimated neurodegeneration model parameters based on individual EEG recordings. RESULTS Our model outperformed standard EEG analysis not only in discriminating between HC and MCI conditions (F1 score 0.95 vs 0.75) but also in identifying SCD patients with biological hallmarks of AD in the cerebrospinal fluid (recall 0.87 vs 0.50). DISCUSSION Personalized models could (1) support classification of MCI, (2) assess the presence of AD pathology, and (3) estimate the risk of cognitive decline progression, based only on economical and non‐invasive EEG recordings. Highlights Personalized cortical model estimating structural alterations from EEG recordings. Discrimination of Mild Cognitive Impairment (MCI) and Healthy (HC) subjects (95%) Prediction of biological markers of Alzheimer's in Subjective Decline (SCD) Subjects (87%) Transition correctly predicted for 3/3 subjects that converted from SCD to MCI after 1y
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
阿尔茨海默病进展的个性化建模可通过脑电图记录估计神经变性的严重程度
摘要 引言 早期识别阿尔茨海默病(AD)对于及时开始治疗非常必要。然而,与阿尔茨海默病相关的皮质结构改变却很难辨别。方法 我们建立了一个与阿兹海默病相关的皮层神经变性模型,该模型考虑了局部动力学减缓和全局连通性退化。在一项单中心研究中,我们收集了健康(HC,n = 17)、主观认知能力下降(SCD,n = 58)和轻度认知障碍(MCI,n = 44)患者静息状态下的脑电图(EEG)记录。我们根据每个患者的脑电图记录估算了神经变性模型参数。结果 我们的模型不仅在区分HC和MCI情况(F1得分0.95 vs 0.75)方面优于标准脑电图分析,而且在识别脑脊液中具有AD生物学特征的SCD患者(召回率0.87 vs 0.50)方面也优于标准脑电图分析。讨论 个性化模型可(1)支持 MCI 分类,(2)评估是否存在 AD 病理,以及(3)仅根据经济和无创的脑电图记录来估计认知能力下降的风险。亮点 通过脑电图记录估计结构改变的个性化皮质模型。鉴别轻度认知功能障碍(MCI)和健康(HC)受试者(95%) 预测主观衰退(SCD)受试者的阿尔茨海默氏症生物标记物(87%) 1 年后从 SCD 转为 MCI 的 3/3 受试者的转归预测正确
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Normative data for the Digit Symbol Substitution for diverse Hispanic/Latino adults: Results from the Study of Latinos‐Investigation of Neurocognitive Aging (SOL‐INCA) Correction to “Retinal microvasculature and incident dementia over 10 years: The Three‐City‐Alienor cohort” Suboptimal self‐reported sleep efficiency and duration are associated with faster accumulation of brain amyloid beta in cognitively unimpaired older adults Social relationships, amyloid burden, and dementia: The ARIC‐PET study Cognitive and functional performance and plasma biomarkers of early Alzheimer's disease in Down syndrome
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1