Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 42, Issue 1, Pages 127-133Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-010-9381-6
Keywords
BACE1; Promoter; Single-nucleotide polymorphisms; Alzheimer's disease
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Funding
- Canadian Institutes of Health Research (CIHR)
- Jack Brown and Family Alzheimer's Research Foundation
- Michael Smith Foundation for Health Research
- Arthur June Willms
- Chinese Scholarship Council
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Alzheimer's disease (AD) is the most neurodegenerative disorder leading to dementia. Neuritic plaque formation in brains is a hallmark of AD pathogenesis. Amyloid beta protein (A beta) is the central component of neuritic plaques. Processing beta-amyloid precursor protein (APP) at the beta-secretase site by the beta-site APP cleaving enzyme 1 (BACE1) is essential for generation of A beta. Elevation of BACE1 activity and expression has been reported in AD brains. However, no mutation in the BACE1 coding sequence has been identified in AD cases. Human BACE1 expression is tightly regulated at the transcription and translation level. To determine whether there is any single-nucleotide polymorphisms in the BACE1 gene promoter region affecting BACE1 expression in AD pathogenesis, in this study, we screened 2.6 kb of the human BACE1 gene promoter region from late-onset AD patients and found that there was no significant association between single-nucleotide polymorphisms and AD cases.
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