How Two Proteins Help Repair Damaged Myelin in the Brain

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Myelin is a fatty substance that wraps around nerve fibers and helps them transmit signals faster and more efficiently. Myelin is essential for normal brain function, but it can be damaged by diseases such as multiple sclerosis or brain injuries. When myelin is damaged, nerve signals are slowed down or disrupted, leading to various neurological symptoms.

Researchers have discovered a new biological mechanism that regulates myelin repair and regeneration in the brain. They found that two proteins, Daam2 and CK2α, play important roles in controlling the development and maturation of the cells that produce myelin, called oligodendrocytes. Their findings could lead to new therapeutic strategies for myelin disorders.

How Two Proteins Help Repair Damaged Myelin in the Brain
How Two Proteins Help Repair Damaged Myelin in the Brain

Daam2 and CK2α: Key Regulators of Myelin Repair

The study was led by Dr. Hyun Kyoung Lee, associate professor of pediatrics – neurology at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. The study was published in the Proceedings of the National Academy of Science.

The researchers focused on a signaling pathway called Wnt, which is known to influence oligodendrocyte development and myelin regeneration. Wnt signaling can have different effects depending on the context and the stage of oligodendrocyte development. In some cases, it can promote the conversion of precursor cells into oligodendrocytes, but in other cases, it can inhibit their maturation and myelination.

The researchers found that Daam2, a protein that is part of the Wnt signaling pathway, acts as a switch that determines the outcome of Wnt signaling. Daam2 can be modified by adding phosphate groups, a process called phosphorylation, which changes its activity and function.

The researchers identified another protein, CK2α, as the enzyme that phosphorylates Daam2. They showed that CK2α interacts with Daam2 in oligodendrocytes and regulates its phosphorylation status.

They also showed that Daam2 phosphorylation has different effects on oligodendrocyte development depending on the stage. In early stages, it accelerates the conversion of precursor cells into oligodendrocytes, but in later stages, it slows down their maturation and myelination.

Implications for Myelin Disorders

The researchers used laboratory cultured oligodendrocytes and mouse models to test the role of Daam2 and CK2α in myelin repair and regeneration. They found that manipulating Daam2 phosphorylation or CK2α activity could enhance or impair myelin production in vitro and in vivo.

These findings suggest that Daam2 and CK2α could be potential targets for modulating myelin repair and regeneration in various neurological conditions that involve myelin damage or loss.

Dr. Lee said: “Our study reveals a new biological mechanism to regulate myelin repair and regeneration by Daam2 phosphorylation mediated by CK2α kinase. We hope that our findings will contribute to the development of novel therapeutic strategies for myelin disorders.”

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