Neuron: New research provides clues to the treatment of neurodegenerative diseases from the roots
March 28, 2017 - For many neurodegenerative diseases, such as Parkinson's disease, amyotrophic lateral sclerosis, and peripheral neuropathy, axonal loss is an early defect. When the axon is lost, the nerve cells cannot communicate properly and the nervous system function is damaged. Especially for peripheral neuropathy, damaged axons trigger a self-destruction procedure.
In a new study, scientists at the University of Washington School of Medicine discovered a special molecule in a self-destructing axon that provides insight into how damage occurs and helps find ways to prevent it from happening.
The relevant research results were published in the international academic journal Neuron.
"Axonal damage occurs in many neurodegenerative diseases. Although these diseases have different causes, they all originate from the same signaling pathway in triggering axonal degeneration. If we can find a way to stop this pathway, it will be Patients with different diseases bring benefits," article author Jeffrey D. Milbrandt said.
Although the role of this molecular pathway leading to axonal loss under normal conditions is not known, scientists believe that if the pathway is suspended or terminated, it will help delay or prevent neurological loss and symptoms. appear.
In previous studies, researchers have found that blocking this axon self-destruction pathway prevents peripheral neuropathy in mice treated with chemotherapy. If the method is applicable to humans, it will be expected to delay or prevent neuropathy in patients receiving chemotherapy.
In this study, the researchers found that a molecule called SARM1 plays an important role in this axonal self-destruction pathway. In healthy axons, SARM1 is present but not activated, and the reason for this is unclear. Injury or disease can activate SARM1, which triggers a series of events that deplete nicotinamide adenine dinucleotide (NAD), a key component of the cell, leading to axonal self-destruction.
The researchers originally thought that SARM1 as a scaffold provided support for the self-destruction process of axons, and the rapid loss of NAD occurred within a few minutes after SARM1 activation. However, the researchers said that after trying a variety of experimental methods, they did not find the classic molecules that consume NAD, and finally they detected SARM1 itself. To their surprise, they found that SARM1 not only provides a platform, but the TIR domain of SARM1 also acts as an enzyme, consuming NAD in cells.
“Many articles are about the function of proteins that contain the TIR domain, but none of them have an enzymatic function. We previously thought that SARM1 is just a scaffold, and there must be other enzymes responsible for consuming NAD. Finally, we discovered that SARM1 itself Playing this role," said another author, Aaron DiAntonio.
These findings suggest that proteins that contain a TIR domain and play a scaffolding role in the immune system may also perform other functions.
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