Linked Life Data

12770611

Source:http://linkedlifedata.com/resource/pubmed/id/12770611

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-5-28
pubmed:abstractText
Amyloid beta protein (Abeta) is the primary constituent of plaque seen in Alzheimer's disease. Abeta is proposed to play an etiological role in Alzheimer's disease and to be a cause of the decrease in the level of acetylcholine in the hippocampus. The SAMP8 strain of mouse develops age-related increases in Abeta and deficits in learning and memory by 12 months of age. We examined in 12 month old SAMP8 mice the effects of giving antibody to Abeta by septal or intracerebroventricular (ICV) injection on acetylcholine levels in the hippocampus. Antibody to Abeta increased acetylcholine in the hippocampus over 100% after ICV injection and over 200% after septal injection. Injection of rabbit serum, antibody directed towards mouse IgG, or a blocking antibody directed towards human interleukin-1beta were without effect. These results suggest that antagonism of Abeta increases acetylcholine concentrations in the hippocampus, an area important for learning and memory.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
555-62
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Antibody to beta-amyloid protein increases acetylcholine in the hippocampus of 12 month SAMP8 male mice.
pubmed:affiliation
Geriatric Research Education and Clinical Center (GRECC), VA Medical Center (151/JC), 915 N. Grand Boulevard, St. Louis, MO 63109, USA. FarrSA52@aol.com
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.