Abstract
We have characterized the myelin changes observed within the hippocampal complex (HC) of a transgenic (Tg) mouse model of Alzheimer’s disease (AD). Individual myelinated fibers were labeled with Black-Gold II while amyloid plaques were labeled with either Congo Red or Pan-A-beta immunofluoresence. Myelinated fibers were never seen passing through amyloid plaques in any region, while conspicuous myelin pathology was seen within, and immediately adjacent to, the amyloid plaques in the HC of the AD-Tg mouse. This pathology consisted of a complete disruption of myelinated fibers passing through the plaque and the region immediately adjacent to the plaques exhibited an edematous swelling of the fibers. This pathology was most frequently observed within the molecular and polymorph layers of the dentate gyrus and the molecular layer of Ammon’s horn. The remaining layers of Ammon’s horn exhibited minimal myelin pathology, while moderate myelinopathy was observed in the subiculum. Since the HC is integral for memory function, these findings may help account for the memory problems so characteristic of the disease process. Because the molecular layers of the dentate gyrus and Ammon’s horn are the sites of inputs to the HC, the extensive myelin pathology observed in these regions would imply functional deafferentation of the HC. The appearance of some Black-Gold II positive debris within the plaques may reflect a possible cascade mechanism whereby the presence of plaques results in myelin degeneration, some of which is incorporated within the plaque, causing it to further expand in a self-perpetuating fashion.
Keywords: Alzheimer’s disease, amyloid plaques, Black-Gold II, demyelination, hippocampus, AD-Tg mouse
Current Alzheimer Research
Title:Characterization of Myelin Pathology in the Hippocampal Complex of a Transgenic Mouse Model of Alzheimer’s Disease
Volume: 10 Issue: 1
Author(s): Larry C. Schmued, James Raymick, Merle G. Paule, Melanie Dumas and Sumit Sarkar
Affiliation:
Keywords: Alzheimer’s disease, amyloid plaques, Black-Gold II, demyelination, hippocampus, AD-Tg mouse
Abstract: We have characterized the myelin changes observed within the hippocampal complex (HC) of a transgenic (Tg) mouse model of Alzheimer’s disease (AD). Individual myelinated fibers were labeled with Black-Gold II while amyloid plaques were labeled with either Congo Red or Pan-A-beta immunofluoresence. Myelinated fibers were never seen passing through amyloid plaques in any region, while conspicuous myelin pathology was seen within, and immediately adjacent to, the amyloid plaques in the HC of the AD-Tg mouse. This pathology consisted of a complete disruption of myelinated fibers passing through the plaque and the region immediately adjacent to the plaques exhibited an edematous swelling of the fibers. This pathology was most frequently observed within the molecular and polymorph layers of the dentate gyrus and the molecular layer of Ammon’s horn. The remaining layers of Ammon’s horn exhibited minimal myelin pathology, while moderate myelinopathy was observed in the subiculum. Since the HC is integral for memory function, these findings may help account for the memory problems so characteristic of the disease process. Because the molecular layers of the dentate gyrus and Ammon’s horn are the sites of inputs to the HC, the extensive myelin pathology observed in these regions would imply functional deafferentation of the HC. The appearance of some Black-Gold II positive debris within the plaques may reflect a possible cascade mechanism whereby the presence of plaques results in myelin degeneration, some of which is incorporated within the plaque, causing it to further expand in a self-perpetuating fashion.
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C. Schmued Larry, Raymick James, G. Paule Merle, Dumas Melanie and Sarkar Sumit, Characterization of Myelin Pathology in the Hippocampal Complex of a Transgenic Mouse Model of Alzheimer’s Disease, Current Alzheimer Research 2013; 10 (1) . https://dx.doi.org/10.2174/1567205011310010005
DOI https://dx.doi.org/10.2174/1567205011310010005 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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