Brain insulation clues emerge in pediatric sleep apnea model, linking myelin changes to motor difficulties

by Graciela Gutierrez, Baylor College of Medicine

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A study published in Experimental Neurology provides new insights into the biological alterations underlying difficulties with precise fine movements observed in pediatric obstructive sleep apnea (POSA).

Researchers at Baylor College of Medicine, Texas Children's Hospital and collaborating institutions worked with a mouse model of POSA that showed deficits in fine motor skills. Their investigation revealed cellular and molecular differences in POSA mice compared with mice without the condition, which may contribute to fine movement impairments in POSA. The findings provide an improved understanding of the condition and an opportunity to develop potential treatments.

"POSA affects about 20% of children," said corresponding author Dr. Arvind Chandrakantan, professor of anesthesiology at Baylor and Texas Children's.

"These children typically feel extremely tired and sleepy during the day—even after getting a full night's sleep. They also show difficulties planning, focusing and remembering instructions and have impulse- and behavior-control issues. They also have difficulties with hand-eye coordination and problems with their mouth, jaw and face that affect their ability to breathe, eat, speak and express emotions."

Because POSA affects children during key periods of growth and development, these impairments have long-term effects on neurodevelopment. For instance, children with impaired movement control show delays in neurodevelopmental milestones such as eating independently and writing.

"Our goal was to characterize cellular and molecular alterations that are associated with POSA in order to identify potential drivers of the condition that may lead to future treatments," Chandrakantan said.

Mouse model mirrors motor deficits

The researchers used a mouse model of POSA they had previously developed. They found that these mice had deficits in fine movements without changes in gross movements, which also is characteristic of children with the condition.

Using imaging techniques, the team confirmed abnormalities in neural connections in various brain regions, which were similar to those observed in children with POSA.

"We then took a closer look at the brains of POSA mice," Chandrakantan said. "Our previous studies had revealed that our mouse model had deficits in the hippocampus and the olfactory bulb. We found fewer neural progenitors and impaired integration into existing neural circuits in these brain regions. We then hypothesized that other brain regions also might be affected in a similar manner."

A closer look at myelin cells

In the current study, the team focused on the corpus callosum (CC), a region located between the brain hemispheres that facilitates communication between them. The CC is essential for key functions such as eating, walking, hand-eye coordination and other fine motor tasks.

The CC has the highest concentration of mature oligodendrocytes, cells that produce myelin, a protective, fatty coating that wraps around nerve fibers. Nerves send electrical signals back and forth between the brain and the rest of the body to control when we move, feel and think. Myelin acts like plastic insulation in an electrical cord; without it, the brain's electrical signals would slow down.

"Efficient high-speed neural signaling is critical for the acquisition and execution of rapid neurodevelopmental motor skills during childhood," Chandrakantan said. "We tested the idea that motor impairments in our model resulted from alterations in oligodendrocytes in the CC."

The researchers found fewer oligodendrocyte progenitor cells (OPCs), with no reduction in mature oligodendrocytes, in the CC of POSA mice relative to normal mice. The decreased functional connectivity they had found earlier was associated with a decrease in OPCs.

Gene changes point to myelination

"Our next step was to look into the genes expressed by oligodendrocytes, and we found many upregulated and downregulated genes involved in the cell's function and differentiation, specifically myelination," Chandrakantan said.

"The CEBPA gene was commonly downregulated in both OPCs and oligodendrocytes in POSA mice. The role of CEBPA in oligodendrocyte differentiation and function has not been investigated in detail and represents a potential future mechanism to be studied."

The findings support the idea that the molecular mechanisms for the disruption of neuronal circuits found in the POSA model involve the loss of myelination, which may contribute to fine motor impairments in POSA.

Future studies using this animal model of POSA could increase understanding of the human condition and lead to treatments that improve outcomes for children with this disease.

Publication details

Mahyar J. Hedayatpour et al, Developmental myelination deficits and impaired fine motor function in a mouse model of pediatric obstructive sleep apnea, Experimental Neurology (2026). DOI: 10.1016/j.expneurol.2026.115991

Journal information: Experimental Neurology

Key medical concepts

Oligodendrocyte Precursor Cellsmyelination

Clinical categories

Sleep medicinePediatricsChildren's healthNeurologySleep & Recovery Provided by Baylor College of Medicine Who's behind this story?

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