Linked Life Data

17027170

Source:http://linkedlifedata.com/resource/pubmed/id/17027170

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-12-4
pubmed:abstractText
Previous studies have described altered expression of metallothioneins (MTs) in neurodegenerative diseases like multiple sclerosis (MS), Down syndrome, and Alzheimer's disease (AD). In order to gain insight into the possible role of MTs in neurodegenerative processes and especially in human diseases, the use of animal models is a valuable tool. Several transgenic mouse models of AD amyloid deposits are currently available. These models express human beta-amyloid precursor protein (AbetaPP) carrying different mutations that subsequently result in a varied pattern of beta-amyloid (Abeta) deposition within the brain. We have evaluated the expression of MT-I and MT-III mRNA by in situ hybridization in three different transgenic mice models of AD: Tg2576 (carrying AbetaPP harboring the Swedish K670N/M671L mutations), TgCRND8 (Swedish and the Indiana V717F mutations), and Tg-SwDI (Swedish and Dutch/Iowa E693Q/D694N mutations). MT-I mRNA levels were induced in all transgenic lines studied, although the pattern of induction differed between the models. In the Tg2576 mice MT-I was weakly upregulated in cells surrounding Congo Red-positive plaques in the cortex and hippocampus. A more potent induction of MT-I was observed in the cortex and hippocampus of the TgCRND8 mice, likely reflecting their higher amyloid plaques content. MT-I upregulation was also more significant in Tg-SwDI mice, especially in the subiculum and hippocampus CA1 area. Immunofluorescence stainings demonstrate that astrocytes and microglia/macrophages surrounding the plaques express MT-I&II. In general, MT-I regulation follows a similar but less potent response than glial fibrillary acidic protein (GFAP) expression. In contrast to MT-I, MT-III mRNA expression was not significantly altered in any of the models examined suggesting that the various MT isoforms may have different roles in these experimental systems, and perhaps also in human AD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
143
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
911-22
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17027170-Alzheimer Disease, pubmed-meshheading:17027170-Amyloid beta-Protein Precursor, pubmed-meshheading:17027170-Animals, pubmed-meshheading:17027170-Astrocytes, pubmed-meshheading:17027170-Brain, pubmed-meshheading:17027170-Cerebral Cortex, pubmed-meshheading:17027170-Disease Models, Animal, pubmed-meshheading:17027170-Female, pubmed-meshheading:17027170-Gene Expression Regulation, Enzymologic, pubmed-meshheading:17027170-Glial Fibrillary Acidic Protein, pubmed-meshheading:17027170-Hippocampus, pubmed-meshheading:17027170-Male, pubmed-meshheading:17027170-Metallothionein, pubmed-meshheading:17027170-Mice, pubmed-meshheading:17027170-Mice, Inbred C57BL, pubmed-meshheading:17027170-Mice, Transgenic, pubmed-meshheading:17027170-Microglia, pubmed-meshheading:17027170-Mutation, pubmed-meshheading:17027170-Nerve Tissue Proteins, pubmed-meshheading:17027170-Plaque, Amyloid, pubmed-meshheading:17027170-RNA, Messenger
pubmed:year
2006
pubmed:articleTitle
Metallothionein-I and -III expression in animal models of Alzheimer disease.
pubmed:affiliation
Institute of Neurosciences, Department of Cellular Biology, Physiology and Immunology, Animal Physiology Unit, Faculty of Sciences, Autonomous University of Barcelona, Bellaterra, Barcelona, Spain 08193.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural