Axonal injury and subsequent neuronal death underpin the pathology of many neurological disorders, from acute neural injuries (motor vehicle crashes, combat-related injuries, traumatic brain injuries) to neurological diseases (multiple sclerosis, glaucoma). In the central nervous system (CNS), microglia help respond to CNS injuries by mediating the immune response and increasing inflammation at the site of injury.  NIH inventors have discovered a novel method for reducing neurodegeneration due to neural injury and possibly other neurodegenerative disorders using Dimethyl Malonate (DMM), a compound that inhibits the activity of succinate dehydrogenase (SDH). This method addresses significant, unmet medical needs since few, if any, treatments exist for neural injuries and neurodegeneration.

Using DMM on an optic nerve crush model in ground squirrels showed that DMM helps reduce the pro-inflammatory response of microglia via decreasing succinate levels or reducing the SDH activity. In the same model, treatment also improved the retinal function compared to controls. Additionally, administering DMM after optic crush injury reduced the microglia response and promoted neural protection against axonal injury. 
 

Competitive advantages of this method include:

• DMM is inexpensive and readily available – reducing manufacturing costs
• Address significant, unmet medical needs since few, if any, treatments exist for neural injuries and neurodegeneration
• Mutation-independent method for treating neurodegeneration

If you are interested in licensing and/or collaborating on this technology, you can view the abstract to learn more or contact a licensing manager: Methods To Regulate Metabolism For Treatment Of Neural Injuries and Neurodegeneration