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Amyloid beta peptide-induced corpus callosum damage and glial activation in vivo.

Authors
Ryu, JK; Kim, SU; McLarnon, JG
Citation
Neuroreport, 14(11):1429-1433, 2003
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
The effects of stereotaxic injection of amyloid beta-peptide (Abeta1-42) into rat brain to induce white matter damage have been studied. Administration of 1 nmol Abeta1-42 into corpus callosum resulted in considerable damage to axons as evidenced by the loss of neurofilament-immunoreactive (NF-ir) fibers 6 h and 3 and 7 days post-injection. Significant damage was also evident to myelin (using Luxol fast blue myelin staining) and oligodendrocytes (using CC1 immunocytochemistry); in the latter case marked caspase-3 immunoreactivity was evident in oligodendrocytes. Additionally, the numbers of GFAP-ir astrocytes and OX-42/OX-6-ir microglia were markedly increased following Abeta1-42 injection. These results suggest that Abeta plays an important pathophysiological role in white matter damage and that inflammatory responses may contribute to Abeta-induced demyelination and oligodendrocyte injury in corpus callosum. Loss of function of cells in corpus callosum could provide a potential new model for the study of white matter damage in Alzheimer's disease.
MeSH terms
Amyloid beta-Peptides/toxicity*AnimalsAstrocytes/drug effectsAstrocytes/pathologyAxons/drug effectsAxons/pathologyColoring AgentsCorpus Callosum/pathology*Glial Fibrillary Acidic Protein/metabolismGliosis/chemically inducedGliosis/pathologyImmunohistochemistryMacrophage Activation/drug effectsMaleMicroscopy, FluorescenceMyelin Sheath/pathologyNerve Fibers/physiologyNeuroglia/drug effects*Neuroglia/pathologyOligodendroglia/physiologyPeptide Fragments/toxicity*RatsRats, Sprague-DawleyStereotaxic Techniques
DOI
10.1097/01.wnr.0000086097.47480.a0
PMID
12960758
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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