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Patient Daily | Mar 30, 2026

Researchers link mild hypoxia in preterm infants to lifelong memory problems

Researchers led by Art Riddle and Stephen Back from Oregon Health and Science University reported on Mar. 23 that mild hypoxia, or low oxygen levels, experienced by preterm infants during intensive care can hinder learning and memory into adulthood.

This finding is important because it helps explain why some children born prematurely face ongoing cognitive challenges, even when they do not suffer obvious brain injuries at birth.

The team created a mouse model to study the effects of mild hypoxia after premature birth. According to Riddle, "The field has historically focused on how hypoxia injures white matter in the brain and kills neurons. This is the first study to explore how mild hypoxia may alter brain development without direct brain injury in this neonatal period." Their research, published in JNeurosci, found that mild hypoxia soon after birth altered neuron-to-neuron communication in the hippocampus—a region critical for memory formation.

Further investigation revealed that a protein channel involved in neuron communication and memory was affected by hypoxia during adolescence. The researchers also identified a second protein influencing this channel's function. By targeting this second protein in adult mice, they were able to restore normal function of the channel. Riddle added, "We also found that this protein was altered by mild hypoxia when we looked at surrounding brain areas, which suggests other brain regions may also be susceptible to hypoxia." The team plans future studies to assess how these additional areas are impacted.

The authors say their work sheds light on how early-life oxygen deprivation influences long-term cognitive outcomes through changes in neuronal communication within memory-related parts of the brain. Discussing potential clinical applications, Riddle said, "The subtle deficits from mild hypoxia that we studied here are commonly seen in clinical settings with preterm babies." Because the molecule identified is not present at the time babies experience hypoxia, future research will focus on earlier developmental molecular targets.

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