Linked Life Data

2960019

Source:http://linkedlifedata.com/resource/pubmed/id/2960019

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4827
pubmed:dateCreated
1987-12-3
pubmed:abstractText
The progressive deposition in the human brain of amyloid filaments composed of the amyloid beta protein is a principal feature of Alzheimer's disease (AD). Densitometric analysis of Southern blots probed with a complementary DNA for the amyloid protein has been carried out to determine the relative dosage of this gene in genomic DNA of 14 patients with AD, 12 aged normal subjects, and 10 patients with trisomy 21 (Down syndrome). Whereas patients in the last group showed the expected 1.5-fold increase in dosage of this gene, none of the patients with AD had a gene dosage higher than that of the normal controls. These results do not support the hypothesis that the genetic defect in AD involves duplication of a segment of chromosome 21 containing the amyloid gene. Alternative mechanisms for the brain-specific increase in amyloid protein deposition in AD should be considered.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
669-71
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Gene dosage of the amyloid beta precursor protein in Alzheimer's disease.
pubmed:affiliation
Department of Neurology, Harvard Medical School, Boston, MA 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't