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Grant: Operating Grant - Priority Announcement: Aging (Bridge Funding)

University of British Columbia

$100,000.00

Regulation of the BACE1 gene expression in the Alzheimer's Disease pathogenesis

FY 2008-09

Summary
Deposition of amyloid beta protein (Abeta) in the brain is a central pathological feature of Alzheimer's disease (AD). Proteolytic processing of beta-amyloid precursor protein (APP) at the beta site by the Beta site APP Cleaving Enzyme 1 (BACE1), the beta-secretase in vivo, is essential to generate Abeta. BACE1 gene expression is tightly regulated and it shows tissue specificity with its enzymatic activity mainly in central nervous system. Increased beta-secretase activity was reported in the cortex of AD patients and abnormal BACE1 gene regulation links vascular factors to AD. We propose to continue studying the molecular mechanisms of BACE1 gene regulation and its role in AD. Our working hypothesis is that transcriptional dysregulation of the BACE1 gene plays an important role in AD pathogenesis. This proposal seeks to further examine transcriptional regulation of the BACE1 gene and the mechanism underlying the 5'UTR regulating BACE1 translation initiation, as well as their role in AD pathogenesis.
Program
Operating Grant - Priority Announcement: Aging (Bridge Funding)
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
175977
Name
Song Weihong
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Molecular & Cellular Neurosciences - B
Projecttitle
Regulation of the BACE1 gene expression in the Alzheimer's Disease pathogenesis
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$100,000
Cihrequipment2
$0
Programname2
Operating Grant - Priority Announcement: Aging (Bridge Funding)
Keyworddelim
Ad Pathogenesis; Alzheimer'S Disease; Amyloid Precursor Protein; Bace1; Gel Shifting Assay; Gene Cloning
Abstract
Deposition of amyloid beta protein (Abeta) in the brain is a central pathological feature of Alzheimer's disease (AD). Proteolytic processing of beta-amyloid precursor protein (APP) at the beta site by the Beta site APP Cleaving Enzyme 1 (BACE1), the beta-secretase in vivo, is essential to generate Abeta. BACE1 gene expression is tightly regulated and it shows tissue specificity with its enzymatic activity mainly in central nervous system. Increased beta-secretase activity was reported in the cortex of AD patients and abnormal BACE1 gene regulation links vascular factors to AD. We propose to continue studying the molecular mechanisms of BACE1 gene regulation and its role in AD. Our working hypothesis is that transcriptional dysregulation of the BACE1 gene plays an important role in AD pathogenesis. This proposal seeks to further examine transcriptional regulation of the BACE1 gene and the mechanism underlying the 5'UTR regulating BACE1 translation initiation, as well as their role in AD pathogenesis.
Competitiondate
200809
Approvedterm2
1 yr 0 mth
Pinamesdelim
Song, Weihong
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $100,000~ $0~