Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-6-27
pubmed:abstractText
Various mutations in the amyloid protein precursor and presenilin genes can lead to early onset, autosomal Alzheimer's disease. A series of mis-sense mutations (with one exception) in each of these genes has been shown to cause disease in a fully penetrant fashion. It has recently been shown, both in vivo and in model systems, that tissues expressing these mutations have increased production of amyloid (A beta) ending at residue 42. It has also recently been shown that this form of A beta is deposited early and selectively in the disease process and is more fibrillogenic in vitro. It is argued that these genetic and molecular biological data provide strong support for the veracity of the 'amyloid cascade hypothesis' for disease pathogenesis, and that this hypothesis offers a coherent framework for drug discovery.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0166-2236
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Amyloid, the presenilins and Alzheimer's disease.
pubmed:affiliation
Mayo Clinic, Jacksonville, FL 32224, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review