Researchers Discover Molecular Switch That Repairs Neurological Damage - Interesting Engineering

Curing disorders such as multiple sclerosis could one day be as simple as turning on a molecular switch thanks to new research by Isobel Scarisbrick, Ph.D., published in the Journal of Neuroscience. Her work finds that by genetically switching off a receptor activated by blood proteins, named Protease Activated Receptor 1 (PAR1), the body switches on regeneration of myelin.

RELATED: NEW MOLECULE LINKED TO STOPPING AND REVERSING NEURO DAMAGE DONE BY PARKINSON’S DISEASE

Improving function

"Myelin regeneration holds tremendous potential to improve function. We showed when we block the PAR1 receptor, neurological healing is much better and happens more quickly. In many cases, the nervous system does have a good capacity for innate repair," said Dr. Scarisbrick, principal investigator, and senior author. "This sets the stage for development of new clinically relevant myelin regeneration strategies."

Myelin is an insulating layer, made up of protein and fatty substances, that forms around nerves, including those in the brain and spinal cord. It protects electrical signals sent through the nervous system. 

Once myelin is injured, electrical signals between brain cells are slowed down. This results in the loss of sensory and motor function you so often see in disorders such as Multiple Sclerosis.

These effects can be cured by thrombin, a protein in blood that aids in healing. However, too much thrombin triggers the PAR1 receptor blocking myelin production. 

Myelin regeneration

The research focused on mice models with myelin injury. When researchers genetically blocked PAR1 to stop the action of excess thrombin, they found a new molecular switch that turns on myelin regeneration.

They also found that a Food and Drug Administration-approved drug that inhibits the PAR1 receptor can also improve myelin production in cells tested in the laboratory.

"It is important to say that we have not and are not advocating that patients take this inhibitor at this time," said Dr. Scarisbrick. "We have not used the drug in animals yet, and it is not ready to put in patients for the purpose of myelin repair. Using cell culture systems, we are showing that this has the potential to improve myelin regeneration.” 

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Wednesday, 01 April 2020

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