New Mouse Models Shed Light on Nerve Damage in Multiple Sclerosis
Multiple sclerosis (MS) is a debilitating neuroinflammatory disease affecting nearly 3 million people worldwide. This disease causes damage to the myelin sheath, the protective covering around nerve cells in the brain and spinal cord. This damage disrupts the flow of nerve impulses, leading to a range of symptoms including fatigue, weakness, vision problems, and cognitive decline.
Understanding the Link Between Myelin Loss and Neuron Damage
While the role of myelin loss in MS is well-established, the exact mechanisms by which this damage leads to neuron death remain a mystery. Now, researchers at OHSU have developed groundbreaking new mouse models that offer crucial insights into this process.
Ben Emery, Ph.D., and Gregory Duncan, Ph.D., have developed new mouse models to confirm the link between failure to repair the protective covering around nerves and loss of neurons. The new models will be useful for not only the Emery lab’s research, but also for other scientists working to address MS and other demyelinating diseases. (OHSU/Christine Torres Hicks)
“Either by pharmacologically or genetically blocking this pathway, we could prevent the death of neurons in these chronically demyelinated mice,” said Ben Emery, Ph.D., corresponding author of the study. Emery is the Warren Distinguished Professor in Neuroscience Research and associate professor of neurology in the OHSU School of Medicine.
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Ben Emery, Ph.D. (OHSU)
Researchers studied two types of mouse models: one that could remyelinate, and one that could not. While both mouse types showed nerve fiber damage, the mice unable to remyelinate experienced significantly more neuron death and inflammation. This underscores the crucial role of new myelin formation in protecting nerve cells from damage.
New Therapeutic Targets for MS
The research also revealed a specific protein pathway closely linked to nerve cell death in mice unable to remyelinate. When researchers blocked this pathway, it effectively prevented neuron loss in these damaged mice.