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

Research output: Contribution to journalShort surveypeer-review

Abstract

Our understanding of the mechanisms whereby BACE1, the aspartyl protease required for the initial cleavage of APP to generate amyloid-β (Aβ), 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 eIF2α 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.

Original languageEnglish (US)
Pages (from-to)941-943
Number of pages3
JournalNeuron
Volume60
Issue number6
DOIs
StatePublished - Dec 26 2008

ASJC Scopus subject areas

  • Neuroscience(all)

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