Source:http://linkedlifedata.com/resource/pubmed/id/17014917
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2006-11-20
|
pubmed:abstractText |
Members of the ADAM family (adisintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid precursor protein within the region of the Abeta peptides preventing their aggregation in the brain. The increase of alpha-secretase activity in the brain provides a plausible strategy to prevent Abeta formation. Concerning this possibility two transgenic mouse lines (FVB/N) have been created: mice over-expressing the bovine form of the alpha-secretase (ADAM10) and mice over-expressing an inactive form of the alpha-secretase (ADAM10-E348A-HA; ADAM10-dn). For behavioral examination a F1 generation of transgenic mice (C57Bl/6 x FVB/N (tg)) was generated and compared to wild type F1 generation (C57Bl/6 x FVB/N). Behavior was characterized in the following tasks: standard open field, enriched open field, elevated plus-maze, and the Morris water maze hidden platform task. Concerning basal activity, exploration, and anxiety, transgenic mice behaved similar to controls. With respect to learning and memory both transgenic lines showed a significant deficit compared to controls. ADAM10 mice however, showed thigmotaxis with passive floating behavior in the Morris water maze indicating differences in motivation, whereas, ADAM10-dn mice displayed an inconspicuous but limited goal-directed search pattern. Thus variation of the enzymatic activity of alpha-secretase ADAM10 alters learning and memory differentially. Nevertheless, it could be concluded that both, ADAM10 and ADAM10-dn mice are suitable control mice for the assessment of alpha-secretase-related effects in animal models of Alzheimer's disease.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0166-4328
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
175
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
278-84
|
pubmed:meshHeading |
pubmed-meshheading:17014917-ADAM Proteins,
pubmed-meshheading:17014917-Amyloid Precursor Protein Secretases,
pubmed-meshheading:17014917-Analysis of Variance,
pubmed-meshheading:17014917-Animals,
pubmed-meshheading:17014917-Anxiety,
pubmed-meshheading:17014917-Behavior, Animal,
pubmed-meshheading:17014917-Exploratory Behavior,
pubmed-meshheading:17014917-Maze Learning,
pubmed-meshheading:17014917-Membrane Proteins,
pubmed-meshheading:17014917-Memory,
pubmed-meshheading:17014917-Mice,
pubmed-meshheading:17014917-Mice, Inbred C57BL,
pubmed-meshheading:17014917-Mice, Transgenic,
pubmed-meshheading:17014917-Motivation
|
pubmed:year |
2006
|
pubmed:articleTitle |
Over-expression of two different forms of the alpha-secretase ADAM10 affects learning and memory in mice.
|
pubmed:affiliation |
Department of Psychiatry, Johannes Gutenberg University, 55101 Mainz, Germany. schmitt@psychiatrie.klinik.uni-mainz.de
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|