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Nucleoredoxin-like 2 metabolic signaling impairs its potential contribution to neurodegenerative diseases

Nucleoredoxin-like 2 metabolic signaling impairs its potential contribution to neurodegenerative diseases

作     者:Mariangela Corsi Céline Jaillard Thierry Léveillard Mariangela Corsi;Céline Jaillard;Thierry Léveillard

作者机构:Sorbonne UniversitéINSERMCNRSInstitut de la VisionParisFrance 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2023年第18卷第3期

页      面:529-530页

核心收录:

学科分类:0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

基  金:funded by the Agence Nationale pour la Recherche Fondation Vaincre Alzheimer and Sorbonne Université 

主  题:approval consequences listed 

摘      要:Alzheimer’s disease(AD)threatens the foundations of humanity and our *** is a neurological disorder primarily affecting the elderly through memory disorders,cognitive decline,and loss of *** dramatic consequences of this late-onset disease were illustrated sensitively in Michael Haneke’s masterpiece,*** and governments have invested colossal efforts to develop a treatment for this terrible *** and in the past decade the amyloid cascade has dominated the therapeutic research on AD,but the absence of benefit for patients treated with drugs that reduce brain amyloid deposit questions the role ofβ-amyloid as a causative agent(Herrup,2021).The recent approval of aducanumab by the United States Food and Drug Administration,a drug that targetsβ-amyloid,is at the center of a scandal among clinicians and researchers,as it does not provide therapeutic benefits to patients and is listed among the breakdowns of the year 2021 by Science magazine(Voosen et al.,2021).The lack of progress in curing AD and recent therapeutic failures calls for further exploratory research.

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