Linked Life Data

18322372

Source:http://linkedlifedata.com/resource/pubmed/id/18322372

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2008-3-6
pubmed:abstractText
Accumulating evidence points to an important role of intraneuronal beta-amyloid (Abeta) in the development of Alzheimer's disease (AD), with its typical clinical symptoms like memory impairment and changes in personality. We have previously reported on the Abeta precursor protein and presenilin-1 knock-out (APP/PS1KI) mouse model with abundant intraneuronal Abeta(42) accumulation and a 50% loss of CA1 neurons at 10 months of age. In addition, we observed reduced short- and long-term synaptic plasticity, hippocampal neuron loss, and reduced performance in a working memory task. These observations support a pivotal role of intraneuronal Abeta accumulation as a principal pathological trigger in AD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1660-2862
pubmed:author
pubmed:copyrightInfo
2008 S. Karger AG, Basel
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
140-2
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Intraneuronal beta-amyloid is a major risk factor--novel evidence from the APP/PS1KI mouse model.
pubmed:affiliation
Department of Psychiatry, Division of Molecular Psychiatry, University of Goettingen, Goettingen, Germany. tbayer@gwdg.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't