Abstract:
: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.
journal_name
Neuronjournal_title
Neuronauthors
Wong PCdoi
10.1016/j.neuron.2008.12.010subject
Has Abstractpub_date
2008-12-26 00:00:00pages
941-3issue
6eissn
0896-6273issn
1097-4199pii
S0896-6273(08)01058-1journal_volume
60pub_type
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