Translational Control of BACE1 May Go Awry in Alzheimer's Disease

被引：14
|
作者：
Wong, Philip C. [1 ,2 ,3 ]
机构：
[1] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Div Neuropathol, Baltimore, MD 21205 USA
来源：
NEURON | 2008年 / 60卷 / 06期
关键词：
D O I：
10.1016/j.neuron.2008.12.010
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Our understanding of the mechanisms whereby BACE1, the aspartyl protease required for the initial cleavage of APP to generate amyloid-beta (A beta), is regulated in Alzheimer's disease (AD) remains incomplete. In this issue of Neuron, O'Connor and coworkers show how energy deprivation, a potential risk factor in AD, triggers the phosphorylation of the translation initiation factor eIF2 alpha to elevate the translation efficiency of a set of stress-related transcripts, including that of BACE1, and increases the level of BACE1, thereby accelerating amyloidogenesis.
引用
收藏
页码：941 / 943
页数：3
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