Novel therapeutic target to treat nerve damage by promoting neuronal survival and regeneration
Inventors: Thomas Schwarz, PhD, Zhigang He, PhD, BM
Invention Types: Therapeutics
Research Areas: Neurology/Neuroscience, Ophthalmology
Keywords: CNS, Neuropathy, Spinal Cord Injury, TargetFor More Information Contact: Ives, Catherine L.
Treating spinal cord and other central nervous system injuries remains a major challenge for neuroscience. These injuries sever axonal connections, which cannot be re-established due to the inability of adult neurons to regenerate. In addition, neuronal loss is major issue common to different types of neurodegenerative diseases.
Zhigang He and Thomas Schwarz have determined that a mitochondrial protein, Armcx1, impacts neuronal survival and axon regeneration after injury. They have shown, using an optic nerve crush injury mouse model, that Armcx1 overexpression in retinal ganglion cells enhances axon survival (A) and regeneration (B). Furthermore, they uncovered that Armcx1 promotes regeneration by increasing mitochondrial transport in injured axons.
These discoveries have revealed a novel target for therapeutic intervention to treat nerve damage and neurodegeneration.
• Novel therapeutic target to stimulate nerve regeneration after spinal cord injury
• Indications could be expanded to many types of nerve damage, from chemotherapy-induced neuropathy to neurodegeneration in diseases such as glaucoma and Alzheimer’s
• Current therapeutic options for spinal cord injury are limited to symptom management (pain killers, rehabilitation) and controversial surgeries
• Armcx1 is a molecular target to potentially reverse nerve damage
Collaboration and Sponsored Research
Key Publications: Cartoni R, et al. The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration. Neuron. 2016 Dec 21;92(6):1294-307.
Cartoni R, et al. A high mitochondrial transport rate characterizes CNS neurons with high axonal regeneration capacity. PLoS One. 2017;12(9):e0184672.
IPStatus: Pat. Pend.