Translational control of BACE1 may go awry in Alzheimer's disease.

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

Neuron

journal_title

Neuron

authors

Wong PC

doi

10.1016/j.neuron.2008.12.010

subject

Has Abstract

pub_date

2008-12-26 00:00:00

pages

941-3

issue

6

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(08)01058-1

journal_volume

60

pub_type

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