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Structure of SARM1 in complex with inhibitor. Credit: Thomas Ve |
The study, led by Griffith University’s Institute for Glycomics and Disarm® Therapeutics, a wholly owned subsidiary of pharmaceutical company Eli Lilly, reveals the structural processes behind activation and inhibition of SARM1, a key molecule in the destruction of nerve fibers.
“As a trigger for nerve fiber degeneration, understanding how the enzyme SARM1 works may help us treat several neurodegenerative conditions,” said Dr Thomas Ve from the Institute for Glycomics.
“In this study we show the molecular interactions that can switch SARM1 on and off. This gives us a clear avenue for the design of new drug therapeutics.”
In neurodegenerative conditions like peripheral neuropathy, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), traumatic brain injury and glaucoma, when the nerve fibers are damaged, SARM1 is activated.
“This sparks a cascade of molecular processes that leads to the self-destruction of the nerve cell’s axon, the cable that carries electric impulse away from the body of the nerve cell to the next,’’ Dr Ve said.