Journal
NEURON
Volume 60, Issue 6, Pages 941-943Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2008.12.010
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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.
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