Microtubule affinity regulating kinase(MARK/Par1)isoforms differentially regulate Alzheimer-like TAU missorting and Aβ-mediated synapse pathology  

作　　者：Jana Chudobová Hans Zempel 

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

出　　处：《Neural Regeneration Research》2023年第2期335-336,共2页中国神经再生研究（英文版）

基　　金：supported by the Koeln Fortune Program/Faculty of Medicine,University of Cologne,the Else-Kr?ner-Fresenius-Stiftung。

摘　　要：Importance of TAU protein for dementia syndromes:Dementia currently affects about 55 million people worldwide,with Alzheimer's disease(AD)being the most prevalent form.The one crucial pathological hallmark of AD that correlates best with loss of synapses and cognitive decline are the so-called intracellular neurofibrillary tangles composed of mislocalized/missorted and hyperphosphorylated TAU protein(Naseri et al.,2019).Many other neurodegenerative diseases,both genetic and nongenetic,are characterized by neurofibrillary ta ngles or pathological accumulation of the protein TAU and are thus termed"tauopathies".

关 键 词：ALZHEIMER diseases 

分 类 号：R749.16[医药卫生—神经病学与精神病学]