Abstract 12- 1030-1045
Category: Basic Science

At the end of the session,
participants will be able to:

  1. Understand the role of the extracellular matrix in the central nervous system in both homeostasis and injury
  2. Learn the alterations in the extracellular matrix in multiple sclerosis and the consequences on disease course

COI Disclosure:

None to disclose


Erin Stephenson is a PGY2 in Neuropathology at the University of Calgary. She completed her MD in 2021 and her PhD in 2018 at the University of Calgary. Her PhD primarily focused on the extracellular matrix of the central nervous system, how it is altered in multiple sclerosis, and the consequences on inflammation.


Erin L. Stephenson1, Samira Ghorbanigazar2, Charlotte D’Mello2, Rajiv William Jain2, V. Wee Yong2. 1. Department of Pathology and Laboratory Medicine, University of Calgary, Calgary AB, Canada 2. Hotchkiss Brain Institute, University of Calgary, Calgary AB, Canada

Target Audience:
Pathologists, Residents, Medical Students

Medical Expert (the integrating role), Collaborator, Health Advocate, Scholar, Professional

The Extracellular Matrix Transcriptome Following Demyelination


The extracellular matrix (ECM) of the central nervous system (CNS) is an interconnected network of proteins and sugars. The ECM has critical roles not only in homeostasis, but ECM remodeling in neurological diseases impacts both injury and repair.
Multiple sclerosis (MS) is a chronic inflammatory and degenerative disease of the CNS. Here, we evaluated ECM changes in MS lesions compared to controls using databases generated in-house through spatial RNA-sequencing, and through a public resource of single-nucleus RNA sequencing. Our results found widespread changes in ECM molecules and their interacting proteins, including alterations to proteoglycans and glycoproteins within inactive and active MS lesions. Some highly upregulated members, including serglycin and SPARC-related proteins, have not previously been investigated and their role on MS lesion evolution and disease course remains unknown. Our results emphasize that there are profound changes to the ECM following demyelination.