Source:http://linkedlifedata.com/resource/pubmed/id/18790549
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
2010-5-18
|
| pubmed:abstractText |
Alzheimer's disease (AD) is characterized by progressive memory impairment and the formation of amyloid plaques in the brain. Dysfunctional excitatory synaptic transmission and synaptic plasticity are generally accepted as primary events in the development of AD, and beta-amyloid is intimately involved. Here we describe age related differences in learning, memory, synaptic transmission and long-term potentiation (LTP) in wild type and APPswe/PS1DeltaE9 mice, which produce increasing amounts of Abeta1-42 with age. The mice have both age related and age-independent deficits in radial arm water maze performance. Blind studies of hippocampal slices from transgenic and wild type mice demonstrate that transgenic mice have impaired transient LTP and that the degree of impairment is not related to age from 3 to 12 months. The deficiencies in transient LTP may be related to the behavioral deficits that did not progress with age. The accumulation of beta-amyloid and the episodic memory deficits, both of which increased with age, were not accompanied by an alteration in synaptic transmission or sustained LTP in the in vitro hippocampal slices.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
1558-1497
|
| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2008 Elsevier Inc. All rights reserved.
|
| pubmed:issnType |
Electronic
|
| pubmed:volume |
31
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1173-87
|
| pubmed:meshHeading |
pubmed-meshheading:18790549-Alzheimer Disease,
pubmed-meshheading:18790549-Amyloid beta-Peptides,
pubmed-meshheading:18790549-Amyloid beta-Protein Precursor,
pubmed-meshheading:18790549-Amyloidosis,
pubmed-meshheading:18790549-Animals,
pubmed-meshheading:18790549-CA1 Region, Hippocampal,
pubmed-meshheading:18790549-Disease Models, Animal,
pubmed-meshheading:18790549-Female,
pubmed-meshheading:18790549-Glutamic Acid,
pubmed-meshheading:18790549-Memory Disorders,
pubmed-meshheading:18790549-Mice,
pubmed-meshheading:18790549-Mice, Inbred C57BL,
pubmed-meshheading:18790549-Mice, Knockout,
pubmed-meshheading:18790549-Mice, Transgenic,
pubmed-meshheading:18790549-Neuronal Plasticity,
pubmed-meshheading:18790549-Organ Culture Techniques,
pubmed-meshheading:18790549-Presenilin-1,
pubmed-meshheading:18790549-Presynaptic Terminals,
pubmed-meshheading:18790549-Synaptic Transmission
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Episodic memory deficits are not related to altered glutamatergic synaptic transmission and plasticity in the CA1 hippocampus of the APPswe/PS1?E9-deleted transgenic mice model of ß-amyloidosis.
|
| pubmed:affiliation |
Institute of Anatomy, University of Aarhus, Denmark.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|