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[Abstract Title]. - Society for Neuroscience

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different MRI scans, clinical global motor score and histopathological data will be conducted. A<br />

methodology based on mechanical measurements of brain structures such as MRE might open<br />

new possibilities <strong>for</strong> the early detection and the management of central demyelinating disorders<br />

such as multiple sclerosis or Alzheimer‟s disease.<br />

Disclosures: E. Diguet , None; B. Larrat, None; M. Fink, None; R. Sinkus, None; E. Yang,<br />

None.<br />

Poster<br />

251. Demyelinating Disorders: Animal Models and Human Studies I<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 251.13/W6<br />

Topic: C.08.b. Animal models<br />

Support: NIH Grant NS39293<br />

DBSCIP Grant F170TP<br />

NMSS Grant RG3515<br />

<strong>Title</strong>: Axonal involvement in early stage cuprizone demyelination of mouse corpus callosum<br />

Authors: *J. E. TOBIN 1 , M. XIE 2 , T. Q. LE 1 , D. MCDANIEL 1 , S.-K. SONG 2 , R. C.<br />

ARMSTRONG 1 ;<br />

1 Anatomy, Physiology,& Genet., USUHS, Bethesda, MD; 2 Washington Univ., St. Louis, MO<br />

<strong>Abstract</strong>: Animal models of demyelinating disease facilitate analysis of pathogenesis and repair<br />

mechanisms as well as development of novel imaging modalities. We used the model of 0.2%<br />

cuprizone fed to adult male C57Bl/6 mice to induce reproducible demyelination of the corpus<br />

callosum (CC). Previously, we demonstrated axonal injury in the CC early in the course of<br />

cuprizone treatment (2 - 6 wks, most extensive at 4 wks) reflected as decreased axial diffusion<br />

measured by diffusion tensor imaging (DTI). Axon damage during this early treatment phase was<br />

also indicated by β-amyloid precursor protein accumulation. In the current study, we more<br />

specifically examined axonal parameters in mice fed cuprizone <strong>for</strong> 4 wks. In vivo DTI of treated<br />

and non-treated mice indicated rostro-caudal differences in pathology from analysis of midline<br />

regions-of-interest taken as 0.5 mm coronal slices encompassing the entire CC. Axial diffusivity<br />

was not altered in the most rostral CC (bregma +1.0 mm) while a significant decrease was seen<br />

in all other regions, with the largest decrease in the most caudal slice (bregma -2.5 mm).<br />

Ultrastructural analysis showed a higher proportion of demyelinated axons in the caudal versus

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