Investigating the Molecule CXCL10 and its Direct Effects on the Central Nervous System in MS

Start Term
End Term
Funding Amount
$299,608
Affiliation(s)
Memorial University of Newfoundland
Geographic Region(s) / Province(s)
Newfoundland and Labrador
Researcher(s)
Research Priorities
Repair/Remyelination
Impact Goal(s)
Understand and Halt Disease Progression

Summary:

  • There is a need for effective treatments that stop disease progression in multiple sclerosis (MS), which is characterized by neurodegeneration due to failure to repair damaged myelin and nerve fibre loss. 
  • Dr. Craig Moore and team have reported a potential role for a molecule called CXCL10 in MS. The team aims to further investigate the mechanisms in which CXCL10 contributes to myelin damage and if it can be reversed. They will also follow a group of people with MS over time to identify if changes to CXCL10 levels in blood correspond to disease progression. 
  • This research has the potential to uncover new mechanisms, biomarkers, and drug targets of MS progression.

Project Description: 
While there are several highly effective disease-modifying therapies for relapsing-remitting MS that target inflammation, these treatments are generally ineffective for progressive MS.

Dr. Craig Moore and team have identified a specific molecule called CXCL10 that is present at high levels in the brain (cerebrospinal fluid and brain lesions) and blood of people with MS. CXCL10 is traditionally known for attracting immune cells (T and B cells) into the brain, thus elevated levels of this compound could contribute to MS pathology. In this study, the researchers will use animal models of MS to explore the mechanisms in which CXCL10 contributes to myelin damage and if it can be reversed. They will also follow a group of people with MS over time to identify potential changes in CXCL10 levels in blood over the course of the disease.

Potential Impact: The findings of this research will uncover new mechanisms, potential biomarkers, and drug targets of MS progression. If CXCL10 is proven to be involved in disease progression, then it can pose as an ideal target to reduce inflammation within the central nervous system while promoting remyelination and repair in MS.

Project Status: In Progress