In vivo and ex vivo diffusion tensor imaging of cuprizone‐induced demyelination in the mouse corpus callosum
Open accessAbstract
Diffusion tensor imaging has been widely used in studying rodent models of white matter diseases. In this study, we examined the differences between in vivo and ex vivo fractional anisotropy and diffusivity measurements in the mouse cuprizone model. In the control mouse corpus callosum, ex vivo diffusivities were significantly lower than in vivo measurements, but ex vivo fractional anisotropy values were not significantly different from in vivo fractional anisotropy values. With cuprizone induced demyelination and accompanying pathology in the corpus callosum, changes in in vivo and ex vivo fractional anisotropy and diffusivity measurements were not always in agreement. Our results suggest that ex vivo λ⟂ was a more reliable indicator of white matter demyelination than in vivo λ⟂ and in vivo λ‖ was a more reliable indicator of axonal injury than ex vivo λ‖ in this model. When comparing in vivo and ex vivo diffusion tensor imaging results of axon and myelin pathology in the rodent models, potential changes in tissue microstructures associated with perfusion fixation should be considered. Magn Reson Med, 2012. © 2011 Wiley Periodicals, Inc.
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Ex vivo FA values differ less from in vivo FA values in the mouse brain.
“But ex vivo FA values differ less from in vivo FA values in the mouse brain (Zhang et al. 2012b).”
From Neurite orientation dispersion and density imaging of mouse brain microstructure (2019) · cites this paper as Zhang et al. 2012b
The Results report no significant in vivo–ex vivo FA difference in the control mouse caudal corpus callosum, even though diffusivity values differed substantially. But they also report a significant FA difference at six weeks of cuprizone treatment. The unqualified claim about the mouse brain therefore extends beyond the conditions supported by the paper (page numbers not provided). (LLM, conf=0.88)
Experimental — accuracy not yet measuredDemyelination is linked to myelin and oligodendrocyte loss, axon damage, active gliosis, and astrocytic hypertrophy.
“Demyelination is linked to myelin and oligodendrocyte loss, axon damage, active gliosis, and astrocytic hypertrophy (Lin et al. 2017; Zhang et al. 2012b; Nikic et al. 2011; Simons et al. 2014; Skripuletz et al. 2008).”
From Neurite orientation dispersion and density imaging of mouse brain microstructure (2019) · cites this paper as Zhang et al. 2012b
The Results report myelin loss, activated microglia and abnormal axonal transport in the cuprizone-treated mouse corpus callosum; the Discussions also report oligodendrocyte death. The paper mentions astrocytes but does not report astrocytic hypertrophy, so that part of the claim is unsupported. Its findings concern this mouse model rather than demyelination generally. (LLM, conf=0.88)
Experimental — accuracy not yet measuredWhile temperature and fixation affect diffusivity values, and ADC in fixed tissue is significantly lower than in vivo, anisotropy values are comparable between in vivo and ex vivo samples.
“While temperature and fixation affect diffusivity values, and ADC in fixed tissue is significantly lower than in vivo (Richardson et al., 2014), anisotropy values are comparable between in vivo and ex vivo samples (Sun et al., 2001, 2003; Zhang et al., 2012).”
From The role of myelination in measures of white matter integrity: Combination of diffusion tensor imaging and two-photon microscopy of CLARITY intact brains (2017) · cites this paper as Zhang et al., 2012
The Discussions report no significant difference between in vivo and ex vivo fractional anisotropy in the normal mouse corpus callosum. But they also report significantly different values in the demyelinated corpus callosum, so the unqualified claim that anisotropy is comparable across samples overextends the finding. (LLM, conf=0.88)
Experimental — accuracy not yet measured
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- Authors
- Zhang, J., Jones, M. V., McMahon, M. T., Mori, S., & Calabresi, P. A.
- Affiliations
- Johns Hopkins University (US)
- Kennedy Krieger Institute (US)
- Corresponding author
- Zhang, Jiangyang
- Venue
- Magnetic Resonance in Medicine
- Publisher
- Wiley
- Published
- 2011-06-07
- Volume
- 67
- Issue
- 3
- Pages
- 750-759
- ISSN
- 0740-3194 (ISSN-L)
- 1522-2594
- PMC
- PMC3170659
- OpenAlex
- W1979250708
- Cited by
- 88
- References
- 40
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 2 · 2023: 6 · 2022: 3 · 2021: 1 · 2020: 6 · 2019: 14 · 2018: 2 · 2017: 6 · 2016: 10 · 2015: 8 · 2014: 9 · 2013: 6 · 2012: 3
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Magnetic Resonance in Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (NS070909, NS059529, NS065306, AG20012, EB003543, ES012665)
- NMSS Collaborative Center Award (NMSS TR-3760-A-3)
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
- Keywords
- cuprizone, demyelination, corpus callosum, diffusion tensor imaging, fractional anisotropy, diffusion coefficient, perfusion fixation, axonal injury, white matter disease, mouse model
- MeSH terms
- Animals, Brain Chemistry, Corpus Callosum, Cuprizone, Demyelinating Diseases, Image Processing, Computer-Assisted, Immunohistochemistry, Mice, Inbred C57BL, Mice, Diffusion Tensor Imaging
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