Source:http://linkedlifedata.com/resource/pubmed/id/15659599
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2005-1-20
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| pubmed:abstractText |
Passive immunization with an antibody directed against the N terminus of amyloid beta (Abeta) has recently been reported to exacerbate cerebral amyloid angiopathy (CAA)-related microhemorrhage in a transgenic animal model. Although the mechanism responsible for the deleterious interaction is unclear, a direct binding event may be required. We characterized the binding properties of several monoclonal anti-Abeta antibodies to deposited Abeta in brain parenchyma and CAA. Biochemical analyses demonstrated that the 3D6 and 10D5, two N-terminally directed antibodies, bound with high affinity to deposited forms of Abeta, whereas 266, a central domain antibody, lacked affinity for deposited Abeta. To determine whether 266 or 3D6 would exacerbate CAA-associated microhemorrhage, we treated aged PDAPP mice with either antibody for 6 weeks. We observed an increase in both the incidence and severity of CAA-associated microhemorrhage when PDAPP transgenic mice were treated with the N-terminally directed 3D6 antibody, whereas mice treated with 266 were unaffected. These results may have important implications for future immune-based therapeutic strategies for Alzheimer's disease.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
1529-2401
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| pubmed:author |
pubmed-author:BalesKelly RKR,
pubmed-author:BooneLaura ILI,
pubmed-author:BrownDonna DDD,
pubmed-author:BryanMatthew TMT,
pubmed-author:DeMattosRonald BRB,
pubmed-author:GitterBruce DBD,
pubmed-author:HepburnDeena LDL,
pubmed-author:HoffmanWherly PWP,
pubmed-author:HoltzmanDavid MDM,
pubmed-author:JordanWilliam HWH,
pubmed-author:MayPatrick CPC,
pubmed-author:NessDaniel KDK,
pubmed-author:ParsadainianMaiaM,
pubmed-author:PaulSteven MSM,
pubmed-author:PirooziKathy SKS,
pubmed-author:RackeMargaret MMM
|
| pubmed:issnType |
Electronic
|
| pubmed:day |
19
|
| pubmed:volume |
25
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
629-36
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:15659599-Aging,
pubmed-meshheading:15659599-Amyloid beta-Peptides,
pubmed-meshheading:15659599-Amyloid beta-Protein Precursor,
pubmed-meshheading:15659599-Animals,
pubmed-meshheading:15659599-Antibody Affinity,
pubmed-meshheading:15659599-Cerebral Amyloid Angiopathy,
pubmed-meshheading:15659599-Cerebral Hemorrhage,
pubmed-meshheading:15659599-Female,
pubmed-meshheading:15659599-Immunization, Passive,
pubmed-meshheading:15659599-Male,
pubmed-meshheading:15659599-Mice,
pubmed-meshheading:15659599-Mice, Transgenic
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Exacerbation of cerebral amyloid angiopathy-associated microhemorrhage in amyloid precursor protein transgenic mice by immunotherapy is dependent on antibody recognition of deposited forms of amyloid beta.
|
| pubmed:affiliation |
Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285, USA.
|
| pubmed:publicationType |
Journal Article
|