The treatment approach is based on an earlier discovery at Washington University in St. Louis, showing that the enzyme SARM1 is a key driver of axon degeneration, a process that causes disability and progression in several diseases of the central, ocular, and peripheral nervous systems.
The discovery was published in the journal Neuron in March 2017. Researchers had earlier known that SARM1 was involved in the degeneration process, but thought that another, so-far unidentified enzyme was needed to perform key steps.
Titled “The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration,” the report showed that SARM1 itself possessed this enzymatic ability, and hence was key in driving neuron death.
“In our recent Neuron publication, we demonstrated that SARM1 itself is the central driver of axonal degeneration,” Jeffrey Milbrandt and Aaron DiAntonio, both MDs and PhDs, co-founders of Disarm Therapeutics from Washington University, said in a press release.
“Importantly, we found that SARM1 possesses an intrinsic enzymatic activity that can be targeted by novel therapeutics,” they added.
SARM1 is involved in a type of axonal degeneration that occurs after injury. The process is a type of programmed self-destruction pathway that affects the axon of an injured cell.
Disarm licensed exclusive rights to SARM1 discoveries from Washington University.
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