Prolonged oxygen exposure may cause long-term memory deficits in preterm infants

Preterm infants often require prolonged oxygen supplementation and are at high risk of neurodevelopmental impairment, according to a study recently published in the journal Nature Scientific Reports. The findings of the study showed that oxygen exposure in newborn mice pups impairs the signalling pathways required for long-term learning and memory formation.

Manimaran Ramani and his associates conducted a study to understand the long-term effect of early oxygen exposure on the development of the brain.

"We are trying to identify therapeutic strategies to prevent and treat cognitive deficits seen in children born preterm and to understand the long-term effects of early oxygen exposure on brain development and function," said Ramani, lead author of the paper. "This study shows that, in mice, oxygen exposure during the critical developmental period may have a deleterious effect on the hippocampal signaling pathway and mitochondrial function—critical needs for the memory formation and maintenance."

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The investigators developed a unique mouse model in which the newborn mice pups were deprived of oxygen and even were not exposed to room air for the first two weeks after birth. After that their cognitive function was studied when they turned adolescents.

As the brain development in the newborn mice pups corresponds to that of 24- to 28-weeks of gestation in human preterm infants, so the novel mouse model will guide the researchers to understand and develop therapies for early oxygen-induced long-term cognitive dysfunction.

The study found that adolescent mice that were exposed to oxygen as neonates had spatial navigation memory deficits and hippocampal shrinkage and the findings that are consistent with children born preterm.

"What this tells us is that oxygen supplementation during the newborn period may have a negative impact long-term brain function," Ramani said. "Since reducing oxygen supplementation is shown to increase the mortality among the preterm infants who require oxygen supplementation, we need to identify the therapies that can mitigate toxic effects of oxygen on brain development and function."

The authors concluded that additional studies are warranted to evaluate the strength of synaptic connections of the hippocampus and to determine the mechanisms by which early oxygen exposure leads to mitochondrial dysfunction in the hippocampus, a brain region that plays an essential role in the formation and maintenance of memory.

For reference log on to https://www.nature.com/articles/s41598-018-28220-4