Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-8-2
pubmed:abstractText
Epidemiological and biochemical data suggest a link between the cholesterol metabolism, the amyloid precursor protein (APP) processing and the increased cerebral beta-amyloid (Abeta) deposition in Alzheimer's disease (AD). The individual and combined effects of a high-cholesterol (HC) diet and the overexpression of the human apoB-100 gene were therefore examined on the cerebral expression and processing of APP in homozygous apoB-100 transgenic mice [Tg (apoB(+/+))], a validated model of atherosclerosis. When fed with 2% cholesterol for 17 weeks, only the wild-type mice exhibited significantly increased APP695 (123%) and APP770 (138%) mRNA levels in the cortex. The HC diet-induced hypercholesterolemia significantly increased the APP isoform levels in the membrane-bound fraction, not only in the wild-type animals (114%), but also in the Tg apoB(+/+) group (171%). The overexpression of human apoB-100 gene by the liver alone reduced the brain APP isoform levels in the membrane-bound fraction (78%), whereas the levels were increased by the combined effect of HC and the overexpression of the human apoB-100 gene (134%). The protein kinase C and beta-secretase protein levels were not altered by the individual or combined effects of these two factors. Our data indicate that the two atherogenic factors, the HC diet and the overexpression of the human apoB-100 gene by the liver, could exert different effects on the processing and expression of APP in the mice brain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid Precursor Protein Secretases, http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Protein Precursor, http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins B, http://linkedlifedata.com/resource/pubmed/chemical/Aspartic Acid Endopeptidases, http://linkedlifedata.com/resource/pubmed/chemical/BACE1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Bace1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, Dietary, http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers, http://linkedlifedata.com/resource/pubmed/chemical/Endopeptidases, http://linkedlifedata.com/resource/pubmed/chemical/Lipids, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0197-0186
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
393-400
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16546298-Amyloid Precursor Protein Secretases, pubmed-meshheading:16546298-Amyloid beta-Protein Precursor, pubmed-meshheading:16546298-Animals, pubmed-meshheading:16546298-Apolipoproteins B, pubmed-meshheading:16546298-Aspartic Acid Endopeptidases, pubmed-meshheading:16546298-Atherosclerosis, pubmed-meshheading:16546298-Blotting, Western, pubmed-meshheading:16546298-Brain Chemistry, pubmed-meshheading:16546298-Cholesterol, pubmed-meshheading:16546298-Cholesterol, Dietary, pubmed-meshheading:16546298-DNA Primers, pubmed-meshheading:16546298-Diet, pubmed-meshheading:16546298-Endopeptidases, pubmed-meshheading:16546298-Female, pubmed-meshheading:16546298-Lipids, pubmed-meshheading:16546298-Mice, pubmed-meshheading:16546298-Mice, Inbred C57BL, pubmed-meshheading:16546298-Mice, Inbred CBA, pubmed-meshheading:16546298-Mice, Transgenic, pubmed-meshheading:16546298-Protein Kinase C, pubmed-meshheading:16546298-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2006
pubmed:articleTitle
Human apoB overexpression and a high-cholesterol diet differently modify the brain APP metabolism in the transgenic mouse model of atherosclerosis.
pubmed:affiliation
Alzheimer's Research Centre, Department of Psychiatry, Albert Szent-Györgyi Center for Medical and Pharmaceutical Sciences, University of Szeged, 6 Semmelweis u., Szeged H-6725, Hungary. a_bjelik@yahoo.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't