Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4-5
pubmed:dateCreated
2006-8-15
pubmed:abstractText
Two enzymatic activities are required to generate the pathogenic beta-amyloid (Abeta) peptide that accumulates in the brain of Alzheimer's disease patients. Both activities are carried out by two unusual aspartyl proteases known as beta- and gamma-secretase. Their therapeutic inhibition appears, therefore, a promising strategy to treat the disease. Transgenic mouse models in which the genes encoding the secretases have been ablated offer an invaluable tool, on the one hand, to gain more insights into the biological function of these proteases and, on the other hand, to predict the consequences that might be associated with enzyme inhibition in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1660-2854
pubmed:author
pubmed:copyrightInfo
Copyright 2004 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
168-74
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
BACE1 and presenilin: two unusual aspartyl proteases involved in Alzheimer's disease.
pubmed:affiliation
Neuronal Cell Biology and Gene Transfer Laboratory, Department of Human Genetics, KU Leuven and VIB4, Leuven, Belgium. Diana-Ines.Dominguez@med.kuleuven.ac.be
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't