Research reported online April 23 in the journal Science presents new insights into the process by which nerves affected by disease of injury begin to die. The discovery suggests new targets for developing drugs that can prevent axons from dying, and slow or halt peripheral neuropathies as well as neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). Peripheral neuropathy damages nerves in the body's extremities and can cause unrelenting pain, stinging, burning, itching, and sensitivity to touch. The condition is commonly associated with diabetes or develops as a side effect of chemotherapy.
Many neurological disorders and traumatic nerve injuries are accompanied by the degeneration of axons, which interrupts nerve signaling and prevents nerves from communicating with one another. Axon degeneration is thought to be an initiating event in many of these disorders, and an unhealthy axon is known to trigger its own death. This study, undertaken by researchers at Washington University School of Medicine in St. Louis identified a protein, SARM1, that once activated, initiates a series of events which quickly causes the axon to self-destruct. But by supplementing the affected cells with a chemical called nicotinamide riboside, the team was able to block axon degeneration and forestall cell death. The results suggest that identifying a class of drugs that block SARM1 activity has therapeutic potential in neurological disorders.
Read a news report about the research findings here.