Scientists Discover an Enzyme That Can Maintain Nerve Function – ZMR Blog
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Scientists Discover an Enzyme That Can Maintain Nerve Function

Scientists Discover an Enzyme That Can Maintain Nerve Function

Axons are an important thread-like part of nerve cells that pass on signals throughout the nervous system. All neuro degenerative diseases involve loss of axons. And now, a research team from the Vollum Institute at OHSU has recognized an enzyme that holds a critical part in the axon degeneration. Thus, this finding can expose new pathways to prevent and treat several brain diseases.A new function was revealed by the scientists of the enzyme Axun dead,also known as Axed, in stimulating axons’ self-destruction. The team found that on blocking the functioning of Axed, the damaged axons not only preserved their integrity, but also stayed capable of conveying signals within the complex circuit of the brain for weeks.

Axotomy, or severing axons, is a simple technique to examine the molecular basis of neuro degeneration as it results in the stimulation of explosive axonal degeneration. With this approach, researchers can recognize pro-degenerative genes in a laboratory with great specificity. In the prior work of Marc Freeman—Director of the Vollum Institute at OHSU—and team, they had found another enzyme, SARM, which was demonstrated to stimulate a course that causes axons to degenerate when injured.

EnzymeNerve Function

In the present study, Freeman and team recognized Axed and demonstrated that it functioned downstream of SARM to perform axonal disintegration, and, startlingly, that the shield given by blocking Axed was even resilient than SARM. From an evolutionary viewpoint, Freeman said,the functions of Axed and SARM are likely essential in the peripheral nervous system after damage as programmed axon death permits for well-organized packing of damaged cellular constituents for elimination by immune cells. This procedure thus frees the way for new neuronal procedures to regrow, reinstate tissues, and recuperate functions.

From a therapeutic viewpoint, the aim of the study is to apprehend at the molecular level the way axons disintegrate and inhibit those pathways to maintain nervous system functioning in patients. Axons are not cut off in many nervous system injuries but are crushed or stretched, which stimulates the SARM-dependent death program and initiates loss of axons. In such conditions, it is essential to inhibit Axed and SARM signaling to maintain axon integrity, and thereby, neuronal function. Simultaneously, the team demonstrated that SARM-dependent signaling pathways also result in loss of axons in neuro degenerative disorders, including traumatic brain injury, peripheral neuropathy, and glaucoma. As axon loss is a common characteristic of neuro degenerative diseases, it appears likely that inhibiting this pathway can have huge therapeutic benefit.

This discovery has given a hope to prevent and treat several neuro degenerative diseases.

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