This invention focuses on peripheral nerve injury prevention and treatment using antibodies, biomolecules, or small molecules.
Peripheral nerve injuries often produce permanent functional deficits despite surgical and medical management. This invention describes a method for preservation of the neuromuscular junction and treatment for peripheral nerve damage.
Researchers at UC Irvine have demonstrated that overexpression of proteoglycan agrin results in motor end plate preservation. Furthermore, the researchers also showed that disruption of matrix metalloproteinase 3 (MMP3) via MMP3 knockout mice resulted in greater endplate efficacy and reinnervation compared to wildtype mice.
Another study done by the inventor showed that after nerve transection injury, elevated levels of proteins Wnt3a and beta catenin are present at the post-synaptic muscle. The WNT/beta-catenin pathway serves as a therapeutic target to prevent motor endplate degradation follow injuries.
The inventors propose a method for nerve injury treatment and prevention by targeting the known protein pathways.
This invention can be used to improve functional nerve recovery after injury. It can also be used for other therapeutic targets based on inhibition of MMP3, Wnt3a, and beta-catenin, and also to stabilize motor endplates.
This technology can be used for treatment, as well as prevention of motor endplate degradation following nerve injury.