Neurodegenerative diseases such as Multiple Sclerosis (MS), Alzheimer's, and Huntington's Disease are predicated on damage to myelin on nerve cells. Myelin smoothes nerve cells so that electrical signals can pass to and from the brain.
New research from Mayo Clinic shows that in mouse models when the Protease Activated Receptor 1 (PAR1) is blocked, the nervous system repairs it's own myelin. The PAR1 receptor produces the protein Thrombin when active, which promotes healing in moderate doses. However, in high doses, Thrombin blocks precursor cells from differentiating into cells that replenish myelin.
The study investigated the effect of blocking PAR1 in mice with short-term and long-term myelin deficiencies, mimicking the effect of different neurodegenerative disorders. In both models, genetically turning off PAR1 was effective in increasing myelin and neuron regeneration.
The Food and Drug Administration has already approved a PAR1 inhibitor for other purposes. Currently, the PAR1 inhibitor is not approved for the treatment of neurodegenerative disorders because the proof of concept has only been tested in animal models, not a clinical setting. Researchers are still excited about the results of this study because if a clinical trial is successful, the treatment can immediately be recommended to patients.