Suppression of mature TAU isoforms prevents Alzheimer's disease-like amyloid-beta oligomer-induced spine loss in rodent neurons
Sarah Buchholz
Hans Zempel
Institute of Human Genetics,Faculty of Medicine and University Hospital Cologne,University of Cologne,Cologne,Germany;Center for Molecular Medicine Cologne(CMMC),Faculty of Medicine and University Hospital Cologne,University of Cologne,Cologne,Germany
摘要:Introduction:TAU isoforms as disease mediators:The microtubule-associated protein TAU is predominantly present in the axons of neurons under physiological conditions.In Alzheimer's disease(AD)and related tauopathies,TAU also mislocalizes("TAU missorting")to the soma and the dendrites,where it eventually forms aggregates,the so-called neurofibrillary tangles(for review see Zimmer-Bensch and Zempel,2021;Zempel,2023).
机标关键词:alzheimerspinelossamyloid-betadisease-likeinducedisoformsmature
论文发表日期:2024-08-28
在线出版日期:2025-08-15(本平台首次上网日期,不代表文献的发表时间)
页数:3( 1655-1657 )
中国神经再生研究(英文版)

中国神经再生研究(英文版)

ISSN:1673-5374
年,卷(期):2024,19(8)
所属栏目:Perspectives