Linked Life Data

15240806

Source:http://linkedlifedata.com/resource/pubmed/id/15240806

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
2004-7-8
pubmed:abstractText
The role of microglia in the removal of amyloid deposits after systemically administered anti-Abeta antibodies remains unclear. In the current study, we injected Tg2576 APP transgenic mice weekly with an anti-Abeta antibody for 1, 2, or 3 months such that all mice were 22 months at the end of the study. In mice immunized for 3 months, we found an improvement in alternation performance in the Y maze. Histologically, we were able to detect mouse IgG bound to congophilic amyloid deposits in those mice treated with the anti-Abeta antibody but not in those treated with a control antibody. We found that Fcgamma receptor expression on microglia was increased after 1 month of treatment, whereas CD45 was increased after 2 months of treatment. Associated with these microglial changes was a reduction in both diffuse and compact amyloid deposits after 2 months of treatment. Interestingly, the microglia markers were reduced to control levels after 3 months of treatment, whereas amyloid levels remained reduced. Serum Abeta levels and anti-Abeta antibody levels were elevated to similar levels at all three survival times in mice given anti-Abeta injections rather than control antibody injections. These data show that the antibody is able to enter the brain and bind to the amyloid deposits, likely opsonizing the Abeta and resulting in Fcgamma receptor-mediated phagocytosis. Together with our earlier work, our data argue that all proposed mechanisms of anti-Abeta antibody-mediated amyloid removal can be simultaneously active.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
7
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6144-51
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15240806-Amyloid, pubmed-meshheading:15240806-Amyloid beta-Peptides, pubmed-meshheading:15240806-Amyloid beta-Protein Precursor, pubmed-meshheading:15240806-Amyloidosis, pubmed-meshheading:15240806-Animals, pubmed-meshheading:15240806-Antibodies, Monoclonal, pubmed-meshheading:15240806-Antigens, CD45, pubmed-meshheading:15240806-Biological Markers, pubmed-meshheading:15240806-Disease Models, Animal, pubmed-meshheading:15240806-Hippocampus, pubmed-meshheading:15240806-Immunization, Passive, pubmed-meshheading:15240806-Immunoglobulin G, pubmed-meshheading:15240806-Immunohistochemistry, pubmed-meshheading:15240806-Maze Learning, pubmed-meshheading:15240806-Mice, pubmed-meshheading:15240806-Mice, Transgenic, pubmed-meshheading:15240806-Microglia, pubmed-meshheading:15240806-Receptors, IgG, pubmed-meshheading:15240806-Time Factors
pubmed:year
2004
pubmed:articleTitle
Passive amyloid immunotherapy clears amyloid and transiently activates microglia in a transgenic mouse model of amyloid deposition.
pubmed:affiliation
Alzheimer's Research Laboratory, University of South Florida, Tampa, Florida 33612, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't