Suppression of mature TAU isoforms prevents Alzheimer's disease-like amyloid-beta oligomer-induced spine loss in rodent neurons  

作　　者：Sarah Buchholz Hans Zempel 

机构地区：[1]Institute of Human Genetics,Faculty of Medicine and University Hospital Cologne,University of Cologne,Cologne,Germany [2]Center for Molecular Medicine Cologne(CMMC),Faculty of Medicine and University Hospital Cologne,University of Cologne,Cologne,Germany

出　　处：《Neural Regeneration Research》2024年第8期1655-1657,共3页中国神经再生研究（英文版）

基　　金：supported by the Deutsche Forschungsgemeinschaft and the Else-Kroner-Fresenius-Stiftung(to HZ)。

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).

关 键 词：Alzheimer Zimmer TAU 

分 类 号：R749.16[医药卫生—神经病学与精神病学]