Modelling Alzheimer's disease using human brain organoids: current progress and challenges.

IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Expert Reviews in Molecular Medicine Pub Date : 2022-12-15 DOI:10.1017/erm.2022.40
Mario Yanakiev, Olivia Soper, Daniel A Berg, Eunchai Kang
{"title":"Modelling Alzheimer's disease using human brain organoids: current progress and challenges.","authors":"Mario Yanakiev,&nbsp;Olivia Soper,&nbsp;Daniel A Berg,&nbsp;Eunchai Kang","doi":"10.1017/erm.2022.40","DOIUrl":null,"url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised by gradual memory loss and declining cognitive and executive functions. AD is the most common cause of dementia, affecting more than 50 million people worldwide, and is a major health concern in society. Despite decades of research, the cause of AD is not well understood and there is no effective curative treatment so far. Therefore, there is an urgent need to increase understanding of AD pathophysiology in the hope of developing a much-needed cure. Dissecting the cellular and molecular mechanisms of AD pathogenesis has been challenging as the most commonly used model systems such as transgenic animals and two-dimensional neuronal culture do not fully recapitulate the pathological hallmarks of AD. The recent advent of three-dimensional human brain organoids confers unique opportunities to study AD in a humanised model system by encapsulating many aspects of AD pathology. In the present review, we summarise the studies of AD using human brain organoids that recapitulate the major pathological components of AD including amyloid-<i>β</i> and tau aggregation, neuroinflammation, mitochondrial dysfunction, oxidative stress and synaptic and circuitry dysregulation. Additionally, the current challenges and future directions of the brain organoids modelling system are discussed.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":"25 ","pages":"e3"},"PeriodicalIF":4.5000,"publicationDate":"2022-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Reviews in Molecular Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1017/erm.2022.40","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 1

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised by gradual memory loss and declining cognitive and executive functions. AD is the most common cause of dementia, affecting more than 50 million people worldwide, and is a major health concern in society. Despite decades of research, the cause of AD is not well understood and there is no effective curative treatment so far. Therefore, there is an urgent need to increase understanding of AD pathophysiology in the hope of developing a much-needed cure. Dissecting the cellular and molecular mechanisms of AD pathogenesis has been challenging as the most commonly used model systems such as transgenic animals and two-dimensional neuronal culture do not fully recapitulate the pathological hallmarks of AD. The recent advent of three-dimensional human brain organoids confers unique opportunities to study AD in a humanised model system by encapsulating many aspects of AD pathology. In the present review, we summarise the studies of AD using human brain organoids that recapitulate the major pathological components of AD including amyloid-β and tau aggregation, neuroinflammation, mitochondrial dysfunction, oxidative stress and synaptic and circuitry dysregulation. Additionally, the current challenges and future directions of the brain organoids modelling system are discussed.

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
用人脑类器官模拟阿尔茨海默病:目前的进展和挑战。
阿尔茨海默病(AD)是一种进行性神经退行性疾病,其特征是逐渐丧失记忆,认知和执行功能下降。阿尔茨海默病是痴呆症的最常见原因,影响着全世界5000多万人,是社会的一个主要健康问题。尽管经过数十年的研究,人们对阿尔茨海默病的病因仍不甚了解,迄今为止也没有有效的治疗方法。因此,迫切需要增加对阿尔茨海默病病理生理的了解,以期开发出急需的治疗方法。解剖阿尔茨海默病发病的细胞和分子机制一直具有挑战性,因为最常用的模型系统,如转基因动物和二维神经元培养,并不能完全概括阿尔茨海默病的病理特征。最近出现的三维人脑类器官通过封装阿尔茨海默病病理的许多方面,为在人性化模型系统中研究阿尔茨海默病提供了独特的机会。在本综述中,我们总结了利用人脑类器官对阿尔茨海默病的研究,这些器官概括了阿尔茨海默病的主要病理成分,包括淀粉样蛋白β和tau聚集、神经炎症、线粒体功能障碍、氧化应激以及突触和电路失调。此外,还讨论了脑类器官建模系统目前面临的挑战和未来的发展方向。
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
Expert Reviews in Molecular Medicine
Expert Reviews in Molecular Medicine BIOCHEMISTRY & MOLECULAR BIOLOGY-MEDICINE, RESEARCH & EXPERIMENTAL
CiteScore
7.40
自引率
1.60%
发文量
45
期刊介绍: Expert Reviews in Molecular Medicine is an innovative online journal featuring authoritative and timely Reviews covering gene therapy, immunotherapeutics, drug design, vaccines, genetic testing, pathogenesis, microbiology, genomics, molecular epidemiology and diagnostic techniques. We especially welcome reviews on translational aspects of molecular medicine, particularly those related to the application of new understanding of the molecular basis of disease to experimental medicine and clinical practice.
期刊最新文献
Cell therapy in Sjögren's syndrome: opportunities and challenges. Radiation drives tertiary lymphoid structures to reshape TME for synergized antitumour immunity. Epigenetic changes in patients with post-acute COVID-19 symptoms (PACS) and long-COVID: A systematic review. Advances in multifunctional metal-organic framework (MOF)-based nanoplatforms for cancer starvation therapy. Thrombocytopenia in dengue infection: mechanisms and a potential application.
×
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