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

Philip C Wong

doi:10.1016/j.neuron.2008.12.010

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

Neuron. 2008 Dec 26;60(6):941-3. doi: 10.1016/j.neuron.2008.12.010.

Author

Philip C Wong¹

Affiliation

¹ Department of Pathology and Neuroscience and the Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. wong@jhmi.edu

PMID: 19109900
DOI: 10.1016/j.neuron.2008.12.010

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.

Publication types

Comment

MeSH terms

Alzheimer Disease / metabolism*
Alzheimer Disease / pathology
Amyloid Precursor Protein Secretases / genetics
Amyloid Precursor Protein Secretases / metabolism*
Amyloid beta-Peptides / metabolism*
Animals
Aspartic Acid Endopeptidases / genetics
Aspartic Acid Endopeptidases / metabolism*
Eukaryotic Initiation Factor-2 / metabolism
Humans
Protein Biosynthesis / physiology
Saccharomyces cerevisiae Proteins / metabolism

Substances

Amyloid beta-Peptides
Eukaryotic Initiation Factor-2
FUN12 protein, S cerevisiae
Saccharomyces cerevisiae Proteins
Amyloid Precursor Protein Secretases
Aspartic Acid Endopeptidases
BACE1 protein, human