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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2011-1-28
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pubmed:abstractText |
The role of amyloid-? (A? in the neurodegeneration of Alzheimer's disease remains controversial, to a large extent because of the lack of robust neurodegeneration in mouse models of AD. To address this question, we examined the effects of A? antibodies in the recently described monoaminergic (MAergic) axonal degeneration in A?PPswe/PS1dE9 mice. To determine if A? accumulation is directly involved in degeneration of MAergic axons, we examined the effects of passive anti-A? antibody (7B6) administration on A? pathology and MAergic degeneration in A?PPswe/PS1dE9 mice. Injections of monoclonal antibody (mAb) 7B6 into mice (6 to 9 months of age) resulted in a modest reduction of A? load in the brains of A?PPswe/PS1dE9 mice. In addition, 7B6 treated A?PPswe/PS1dE9 mice had significantly higher densities of MAergic axons in both cortex and in hippocampus as compared to untreated mutant mice. For example, 7B6 treated mice showed almost 2-fold greater densities of serotonergic (5-HT) axons in the cortex compared to saline treated mice. Similar findings were observed in the catecholaminergic (TH) axons. Our results demonstrate that lowering of A? levels via passive A? immunotherapy ameliorates ongoing degenerative processes, supporting a causal link between A? and neurodegeneration.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-11123722,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-11160418,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-11198297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-11337275,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-12130773,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-12493547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-14645482,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-15282285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-15475950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-15668737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-15707619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-16228992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-16567017,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-16574280,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-1672782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-18091561,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-18352830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-18568035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-18640458,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-19091971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-19228947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-20083042,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-3178178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-9278541,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-9291938,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20966549-9530504
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:issn |
1875-8908
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
271-9
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pubmed:dateRevised |
2011-7-27
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pubmed:meshHeading |
pubmed-meshheading:20966549-Alzheimer Disease,
pubmed-meshheading:20966549-Amyloid beta-Peptides,
pubmed-meshheading:20966549-Amyloid beta-Protein Precursor,
pubmed-meshheading:20966549-Animals,
pubmed-meshheading:20966549-Antibodies, Monoclonal,
pubmed-meshheading:20966549-Axons,
pubmed-meshheading:20966549-Biogenic Monoamines,
pubmed-meshheading:20966549-Brain,
pubmed-meshheading:20966549-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20966549-Immunization, Passive,
pubmed-meshheading:20966549-Immunohistochemistry,
pubmed-meshheading:20966549-Mice,
pubmed-meshheading:20966549-Mice, Transgenic,
pubmed-meshheading:20966549-Nerve Degeneration,
pubmed-meshheading:20966549-Statistics, Nonparametric
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pubmed:year |
2011
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pubmed:articleTitle |
Passive (amyloid-?) immunotherapy attenuates monoaminergic axonal degeneration in the A?PPswe/PS1dE9 mice.
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pubmed:affiliation |
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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