Release date: 2017-07-18
Scientists at the OHSU Vollum Institute have discovered an enzyme that plays a key role in the axonal degeneration of the linear portions of nerve cells that transmit signals in the nervous system. Axonal loss occurs in all neurodegenerative diseases, so this finding opens up new avenues for treating or preventing a wide range of brain diseases.
The team found that Axendead or Axed enzymes play a new role in promoting axonal destruction. They found that when the Axed function was blocked, the injured axon not only maintained its integrity, but was still able to transmit signals for several weeks in complex circuits in the brain. Their research was published in the journal Neuron on July 5.
Dr. Marc Freeman, Director of the OHSU Vollum Institute, said: "If you aim at this pathway, you will have the opportunity to preserve the function of neurons after various traumas or injuries. "This is a very attractive therapeutic goal. â€
Freeman worked at the Department of Neurobiology at the University of Massachusetts School of Medicine. He has been recruited to lead the Vollum Institute to conduct cutting-edge basic research on the work of the nervous system at the molecular level.
Axotomy or axotomy is the molecular basis for studying neurodegeneration because it leads to the activation of explosive axonal degeneration as a simple method. In the laboratory, researchers using this technique can identify the original degenerative genes, especially when using complex genetic methods in Drosophila, Freeman's main research model organism. Drosophila shares these same pathways with humans. Previous work at Freeman Lab identified another enzyme, a gene called SARM, which is the first demonstration of activation of a process that causes axons to break down during injury.
In the current study, Freeman and colleagues found that Axed works downstream of SARM to perform axonal degeneration, and surprisingly, blocking Axed provides greater protection than SARM.
Freeman said: "In the place where Axed functionality is blocked, we have nothing to do.
Freeman believes that from an evolutionary perspective, SARM and Axed functions may be important in the peripheral nervous system after injury, because programmed axonal death can effectively package damaged cell material to avoid cell removal. Therefore, this process clears the way in which new neuronal processes regenerate, restore tissue and restore function.
From a therapeutic point of view, the goal of the work is to understand how the axons degenerate at the molecular level and to prevent these pathways in the patient from protecting the function of the nervous system. In many neurological injuries, axons are not severed but are stretched or crushed, which activates the SARM-dependent death program and drives axonal loss. In these cases, the SARM and Axed signals must be blocked to protect the axonal integrity. At the same time, Freeman et al. have shown that SARM-dependent signaling pathways can also drive axonal loss in neurodegenerative diseases including glaucoma, traumatic brain injury and peripheral neuropathy. This suggests that an ancient and conserved axonal death signaling pathway is widely activated to drive the concept of axonal loss. Since axonal loss is a common feature of neurodegenerative diseases, it seems that preventing this pathway may have a huge therapeutic effect.
Freeman said: "If we can find a way to stop it, maybe we can retain function in many patients with axonal damage through neurodegenerative diseases or other neurological trauma.
Source: Noble
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