Neuronal system for maintaining brain myelin identified ... raising hopes for brain disease treatments [Health LAB]

[Financial News] A molecular signaling system through which neurons maintain myelin in the brain has been identified. The finding raises hopes that the research could be expanded to include studies of new treatment strategies to promote the repair of myelin damage caused by aging and neurodegenerative brain diseases.
According to the Korea Brain Research Institute on the 23rd, a research team led by Choi Young-sik, a principal researcher in the institute’s Department of Brain Disease Research, identified a new molecular signaling system through which neurons regulate oligodendrocyte maturation to stably maintain myelin in the adult brain.
Myelin is an insulating structure that surrounds the axons of neurons and is essential for the fast and stable transmission of nerve signals. However, it has not been fully understood what signals neurons use to maintain myelin in the adult brain.
The team found that FAM19A1, a protein secreted by neurons in the central nervous system, plays an important role in stably maintaining myelin structures that have already formed in the adult brain. Proteomic analysis also identified DIP2A, found on the surface of oligodendrocytes, as a receptor for FAM19A1. When the team selectively suppressed Dip2a expression in oligodendrocytes in the brains of adult mice, myelin in the corpus callosum decreased, confirming that FAM19A1-DIP2A signaling plays an important role in oligodendrocyte maturation and the maintenance of myelin in adults.
The team went a step further and discovered a molecular switch through which neurons regulate FAM19A1 secretion. When CDK14, a protein kinase in neurons, phosphorylates threonine (T109), the 109th amino acid of FAM19A1, FAM19A1 secretion is promoted and its binding to DIP2A is strengthened. Conversely, when this process is blocked, FAM19A1 secretion and its binding to DIP2A decrease, as does its ability to promote oligodendrocyte maturation.
In other words, a signaling sequence exists in which neuronal CDK14 phosphorylates FAM19A1 and promotes its secretion, after which the secreted FAM19A1 binds to DIP2A on oligodendrocytes to promote cell maturation and myelin maintenance. The study presents a new principle of neuron-glia interaction: neurons do not merely receive protection from myelin, but actively regulate the state of surrounding oligodendrocytes to maintain their own myelin environment.
Corresponding author Dr. Choi Young-sik said, “We confirmed that neurons are not merely protected by myelin, but actively regulate oligodendrocyte maturation and the state of myelin using a molecular signal called FAM19A1,” adding, “If future research clarifies how the CDK14-FAM19A1-DIP2A signaling axis is related to myelin damage caused by aging and neurodegenerative brain diseases, it could lead to research into new treatment strategies to preserve the stability of myelin in adults or promote the repair of damaged myelin.”
The study was published in the international journal Cell Communication and Signaling.

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