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Regulation of β‐site APP‐cleaving enzyme 1 gene expression and its role in Alzheimer’s Disease
Author(s) -
Sun Xiulian,
BromleyBrits Kelley,
Song Weihong
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07515.x
Subject(s) - senile plaques , bace1 as , pathogenesis , amyloid precursor protein , neuropathology , alzheimer's disease , amyloid precursor protein secretase , translation (biology) , biology , gene expression , neuroscience , regulation of gene expression , disease , gene , alpha secretase , medicine , messenger rna , genetics , pathology , immunology
J. Neurochem. (2012) 120 (Suppl. 1), 62–70. Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disorder leading to dementia. Neuritic plaques are the hallmark neuropathology in AD brains. Proteolytic processing of amyloid‐β precursor protein at the β site by beta‐site amyloid‐β precursor protein‐cleaving enzyme 1 (BACE1) is essential to generate Aβ, a central component of the neuritic plaques. BACE1 is increased in some sporadic AD brains, and dysregulation of BACE1 gene expression plays an important role in AD pathogenesis. This review will focus on the regulation of BACE1 gene expression at the transcriptional, post‐transcriptional, translation initiation, translational and post‐translational levels, and its role in AD pathogenesis. Further studies on BACE1 gene expression regulation will greatly contribute to our understanding of AD pathogenesis and reveal potential novel approaches for AD prevention and drug development.