TY - JOUR
T1 - Translational Control of BACE1 May Go Awry in Alzheimer's Disease
AU - Wong, Philip C.
PY - 2008/12/26
Y1 - 2008/12/26
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=57649225077&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57649225077&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2008.12.010
DO - 10.1016/j.neuron.2008.12.010
M3 - Short survey
C2 - 19109900
AN - SCOPUS:57649225077
SN - 0896-6273
VL - 60
SP - 941
EP - 943
JO - Neuron
JF - Neuron
IS - 6
ER -