Linked Life Data

20455082

Source:http://linkedlifedata.com/resource/pubmed/id/20455082

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-8-2
pubmed:abstractText
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 (Abeta) 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 Abeta. 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1559-1166
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-33
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
BACE1 gene promoter single-nucleotide polymorphisms in Alzheimer's disease.
pubmed:affiliation
Townsend Family Laboratories, Department of Psychiatry, Brain Research Center, Graduate Program in Neuroscience, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T1Z3, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural