Translational Control of BACE1 May Go Awry in Alzheimer's Disease
نویسنده
چکیده
Our understanding of the mechanisms whereby BACE1, the aspartyl protease required for the initial cleavage of APP to generate amyloid-beta (Abeta), 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 eIF2alpha 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.
منابع مشابه
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عنوان ژورنال:
- Neuron
دوره 60 شماره
صفحات -
تاریخ انتشار 2008