Linked Life Data

17499931

Source:http://linkedlifedata.com/resource/pubmed/id/17499931

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-6-11
pubmed:abstractText
Alzheimer's disease is characterized by the presence of senile plaques in the brain, composed mainly of aggregated amyloid-beta peptide (Abeta), which plays a central role in the pathogenesis of Alzheimer's disease and is a potential target for therapeutic intervention. Amyloid plaques occur in an increasing number of brain structures during the progression of the disease, with a heavy load in regions of the temporal cortex in the early phases. Here, we investigated the cognitive deficits specifically associated with amyloid pathology in the entorhinal cortex. The amyloid peptide Abeta(1-42) was injected bilaterally into the entorhinal cortex of rats and behavioral performance was assessed between 10 and 17 days after injection. We found that parameters of motor behavior in an open-field as well as spatial working memory tested in an alternation task were normal. In contrast, compared with naive rats or control rats injected with saline, rats injected with Abeta(1-42) showed impaired recognition memory in an object recognition task and delayed acquisition in a spatial reference memory task in a water-maze, despite improved performance with training in this task and normal spatial memory in a probe test given 24 h after training. This profile of behavioral deficits after injection of Abeta(1-42) into the entorhinal cortex was similar to that observed in another group of rats injected with the excitotoxic drug, N-methyl-d-aspartate. Immunohistochemical analysis after behavioral testing revealed that Abeta(1-42) injection induced a reactive astroglial response and plaque-like deposits in the entorhinal cortex. These results show that experimentally-induced amyloid pathology in the entorhinal cortex induces selective cognitive deficits, resembling those observed in early phases of Alzheimer's disease. Therefore, injection of protofibrillar-fibrillar Abeta(1-42) into the entorhinal cortex constitutes a promising animal model for investigating selective aspects of Alzheimer's disease and for screening drug candidates designed against Abeta pathology.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28-36
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17499931-Alzheimer Disease, pubmed-meshheading:17499931-Amyloid beta-Peptides, pubmed-meshheading:17499931-Animals, pubmed-meshheading:17499931-Cognition Disorders, pubmed-meshheading:17499931-Disease Models, Animal, pubmed-meshheading:17499931-Entorhinal Cortex, pubmed-meshheading:17499931-Exploratory Behavior, pubmed-meshheading:17499931-Gliosis, pubmed-meshheading:17499931-Male, pubmed-meshheading:17499931-Maze Learning, pubmed-meshheading:17499931-Microinjections, pubmed-meshheading:17499931-N-Methylaspartate, pubmed-meshheading:17499931-Neurotoxins, pubmed-meshheading:17499931-Peptide Fragments, pubmed-meshheading:17499931-Plaque, Amyloid, pubmed-meshheading:17499931-Rats, pubmed-meshheading:17499931-Rats, Wistar, pubmed-meshheading:17499931-Recognition (Psychology), pubmed-meshheading:17499931-Statistics, Nonparametric
pubmed:year
2007
pubmed:articleTitle
Beta-amyloid pathology in the entorhinal cortex of rats induces memory deficits: implications for Alzheimer's disease.
pubmed:affiliation
University of Szeged, Institute of Medical Chemistry, Dóm tér 8., H-6720 Szeged, Hungary. bodonesiposeszter@gmail.com
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't