Graciela Gutierrez

713-798-4710

Houston, TX - Sep 10, 2026

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A study published in Experimental Neurology provides new insights into the biological alterations underlying the 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 when compared to mice without the condition, which may contribute to the 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 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.

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."

In the current study, the team focused on the corpus callosum (CC), a region located between the brain hemispheres that facilitates communication between them. 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 neurodevelopment 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 oligodendrocytes 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.

"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 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 offer the possibility of increasing our understanding of the human condition and of future treatments to improve the outcomes of children with this disease.

Other contributors to this work include Mahyar J. Hedayatpour, Roshan Ailani, Michael R. Williamson, Steen Erik Pedersen, Robia Pautler, Mathilda S. Nicot-Cartsonis, Adam C. Adler, Farrah Kheradmand, Benjamin Deneen, Akdes Serin Harmanci and Hyun Kyoung Lee. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine, Texas Children's Hospital, Michael E. DeBakey VA - Houston, the Hospital for Sick Children - Toronto and the University of Toronto.

The study was supported by the following grants: 1F31NS145624-01, K08HL161263, 25POST1363224 and 2R01NS118059.