The phosphorylation cascade hypothesis of Alzheimer's disease

被引：7
|
作者：
Brinkmalm, Gunnar [1 ,2 ]
Zetterberg, Henrik [1 ,2 ,3 ,4 ]
机构：
[1] Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Molndal, Sweden
[2] Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden
[3] UCL Queen Sq Inst Neurol, Dept Neurodegenerat Dis, London, England
[4] UCL, UK Dementia Res Inst, London, England
来源：
NATURE AGING | 2021年 / 1卷 / 06期
关键词：
D O I：
10.1038/s43587-021-00077-9
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Alzheimer's disease (AD) is characterized by amyloid-beta (A beta)-induced phosphorylation of the axon-stabilizing tau protein, which causes neurodegeneration. Here, Morshed et al. show that deregulated phosphorylation in AD also affects other proteins and cell types in the brain, suggesting that the tau-centric view on A beta toxicity should be revised.
引用
收藏
页码：498 / 499
页数：2
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