Jie Liu, Heleen van Beusekom, Xian‐Le Bu, Gong Chen, Paulo Henrique Rosado de Castro, Xiaochun Chen, Xiaowei Chen, Andrew N. Clarkson, Tracy D. Farr, Yuhong Fu, Jianping Jia, Jukka Jolkkonen, Woojin Scott Kim, Paula Korhonen, Shen Li, Yajie Liang, Guang‐Hui Liu, Guiyou Liu, Yu‐Hui Liu, Tarja Malm, Xiaobo Mao, Joaquim Miguel Oliveira, Mike M. Modo, Pedro Ramos‐Cabrer, Karsten Ruscher, Weihong Song, Jun Wang, Xuanyue Wang, Yun Wang, Haitao Wu, Lize Xiong, Yi Yang, Keqiang Ye, Jin‐Tai Yu, Xin‐Fu Zhou, Marietta Zille, Colin L. Masters, Piotr Walczak, Boltze Johannes, Xunming Ji, Yan‐Jiang Wang
{"title":"Preserving cognitive function in patients with Alzheimer's disease: The Alzheimer's disease neuroprotection research initiative (ADNRI)","authors":"Jie Liu, Heleen van Beusekom, Xian‐Le Bu, Gong Chen, Paulo Henrique Rosado de Castro, Xiaochun Chen, Xiaowei Chen, Andrew N. Clarkson, Tracy D. Farr, Yuhong Fu, Jianping Jia, Jukka Jolkkonen, Woojin Scott Kim, Paula Korhonen, Shen Li, Yajie Liang, Guang‐Hui Liu, Guiyou Liu, Yu‐Hui Liu, Tarja Malm, Xiaobo Mao, Joaquim Miguel Oliveira, Mike M. Modo, Pedro Ramos‐Cabrer, Karsten Ruscher, Weihong Song, Jun Wang, Xuanyue Wang, Yun Wang, Haitao Wu, Lize Xiong, Yi Yang, Keqiang Ye, Jin‐Tai Yu, Xin‐Fu Zhou, Marietta Zille, Colin L. Masters, Piotr Walczak, Boltze Johannes, Xunming Ji, Yan‐Jiang Wang","doi":"10.1002/nep3.23","DOIUrl":null,"url":null,"abstract":"Abstract The global trend toward aging populations has resulted in an increase in the occurrence of Alzheimer's disease (AD) and associated socioeconomic burdens. Abnormal metabolism of amyloid‐β (Aβ) has been proposed as a significant pathomechanism in AD, supported by results of recent clinical trials using anti‐Aβ antibodies. Nonetheless, the cognitive benefits of the current treatments are limited. The etiology of AD is multifactorial, encompassing Aβ and tau accumulation, neuroinflammation, demyelination, vascular dysfunction, and comorbidities, which collectively lead to widespread neurodegeneration in the brain and cognitive impairment. Hence, solely removing Aβ from the brain may be insufficient to combat neurodegeneration and preserve cognition. To attain effective treatment for AD, it is necessary to (1) conduct extensive research on various mechanisms that cause neurodegeneration, including advances in neuroimaging techniques for earlier detection and a more precise characterization of molecular events at scales ranging from cellular to the full system level; (2) identify neuroprotective intervention targets against different neurodegeneration mechanisms; and (3) discover novel and optimal combinations of neuroprotective intervention strategies to maintain cognitive function in AD patients. The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated, multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD. The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD, with the goal of halting or even reversing cognitive decline.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"8 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroprotection","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/nep3.23","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Abstract The global trend toward aging populations has resulted in an increase in the occurrence of Alzheimer's disease (AD) and associated socioeconomic burdens. Abnormal metabolism of amyloid‐β (Aβ) has been proposed as a significant pathomechanism in AD, supported by results of recent clinical trials using anti‐Aβ antibodies. Nonetheless, the cognitive benefits of the current treatments are limited. The etiology of AD is multifactorial, encompassing Aβ and tau accumulation, neuroinflammation, demyelination, vascular dysfunction, and comorbidities, which collectively lead to widespread neurodegeneration in the brain and cognitive impairment. Hence, solely removing Aβ from the brain may be insufficient to combat neurodegeneration and preserve cognition. To attain effective treatment for AD, it is necessary to (1) conduct extensive research on various mechanisms that cause neurodegeneration, including advances in neuroimaging techniques for earlier detection and a more precise characterization of molecular events at scales ranging from cellular to the full system level; (2) identify neuroprotective intervention targets against different neurodegeneration mechanisms; and (3) discover novel and optimal combinations of neuroprotective intervention strategies to maintain cognitive function in AD patients. The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated, multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD. The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD, with the goal of halting or even reversing cognitive decline.
人口老龄化的全球趋势导致阿尔茨海默病(AD)发病率的增加和相关的社会经济负担。淀粉样蛋白β (a β)代谢异常被认为是AD的一个重要病理机制,最近使用抗a β抗体的临床试验结果也支持了这一观点。尽管如此,目前的治疗方法对认知的好处是有限的。AD的病因是多因素的,包括Aβ和tau积聚、神经炎症、脱髓鞘、血管功能障碍和合并症,这些因素共同导致广泛的大脑神经变性和认知障碍。因此,仅仅从大脑中去除Aβ可能不足以对抗神经变性和保持认知。为了获得对AD的有效治疗,有必要(1)对导致神经退行性变的各种机制进行广泛的研究,包括神经成像技术的早期检测和更精确地表征从细胞到全系统水平的分子事件;(2)确定针对不同神经退行性变机制的神经保护干预靶点;(3)发现新的和最佳的神经保护干预策略组合,以维持AD患者的认知功能。阿尔茨海默病神经保护研究倡议的目标是促进协调,多学科的努力,以制定系统的神经保护策略,以对抗AD。目的是减轻阿尔茨海默病的所有病理过程,目标是停止甚至逆转认知能力下降。