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Related Experiment Video

Updated: Feb 12, 2026

A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
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Exploring experimental autoimmune optic neuritis using multimodal imaging.

Praveena Manogaran1, Christine Walker-Egger2, Marijana Samardzija3

  • 1Neuroimmunology and Multiple Sclerosis Research, Clinic for Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland; Department of Information Technology and Electrical Engineering, Swiss Federal Institute of Technology, Zurich, Switzerland.

Neuroimage
|April 9, 2018
PubMed
Summary
This summary is machine-generated.

Neuro-axonal injury in multiple sclerosis (MS) is studied using optical coherence tomography (OCT) and diffusion tensor imaging (DTI) in a rodent model. Findings reveal inflammatory edema followed by neurodegeneration in the visual pathway.

Keywords:
Diffusion tensor imagingExperimental autoimmune encephalomyelitisNeuro-axonal degenerationOptic neuritisOptical coherence tomographyRetina

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Immunology

Background:

  • Neuro-axonal injury is a primary cause of irreversible disability in multiple sclerosis (MS).
  • Visual impairment, including optic neuritis (ON), is common in MS, leading to retinal damage and functional loss.
  • The animal model of MS, experimental autoimmune encephalomyelitis (EAE), exhibits optic nerve and retinal alterations, making it suitable for studying neurodegeneration mechanisms.

Purpose of the Study:

  • To investigate the mechanisms and temporal dynamics of visual pathway damage in an animal model of MS.
  • To utilize a multimodal imaging approach combining optical coherence tomography (OCT) and diffusion tensor imaging (DTI).
  • To explore structural changes in the anterior visual pathway as a model for MS neurodegeneration.

Main Methods:

  • Used 7 EAE mice and 5 controls, employing OCT for ganglion cell complex (GCC) thickness and DTI/MRI for optic nerve and tract structure.
  • Acquired data at baseline, disease onset, peak, and recovery, analyzing with linear mixed effect models.
  • Correlated GCC thickness with DTI parameters (AD, RD) and used immunofluorescence for microglia, astrocytosis, and axonal degeneration markers.

Main Results:

  • EAE mice showed increased GCC thickness at onset, followed by significant thinning at recovery compared to controls.
  • DTI revealed decreased axial diffusivity (AD) and increased radial diffusivity (RD) in optic nerves and tracts of EAE mice.
  • Immunofluorescence confirmed activated microglia, astrocytosis, and axonal degeneration in the optic nerve of EAE mice.

Conclusions:

  • OCT findings in EAE mice mimic MS-related ON, showing initial swelling and subsequent thinning indicative of neuro-axonal degeneration.
  • DTI successfully identified EAE-induced pathology in the visual pathway, correlating with OCT and immunofluorescence results.
  • OCT and DTI provide in vivo detection of retinal and optic nerve damage, elucidating the temporal sequence of neurodegeneration in MS models.