Each year, thousands of newborn babies suffer complications during pregnancy or birth that deprive their brains of oxygen and nutrient-rich blood and result in brain injury.
This deprivation causes hypoxic ischemic encephalopathy (HIE), which can lead to long-term neurological issues such as learning disabilities, cerebral palsy or even death.
Researchers have known for some time that male infants are more vulnerable to HIE than females, but why this gender difference exists has remained a mystery.
"People often think that biological sex differences start to arise only after puberty, but they actually start in the womb and persist until the tomb," said Cengiz.
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"So, treatment approaches that may work for newborn boys may not work for girls, and vice versa. We need to get it right to develop effective therapies," Cengiz said.
The drug works by turning on a cascade of protective effects in the brain in response to oxygen deprivation and reduced blood flow.
Researchers found that, like the drug, ERa also causes a similar cascade in infant mice and the protein is actually required for the drug to be effective.
They found that female mice lacking the ERa protein could not activate protective factors following HIE, even when treated with the drug.
"Under normal circumstances the brains of male and female mice have similar amounts of ERa," said Cengiz, who is now exploring why ERa levels increase in female but not male brains after HIE.
Understanding the mechanism of how female brains are more resistant to damage from oxygen deprivation and reduced blood flow is a first step towards helping newborns of both sexes recover after suffering from HIE and live functional lives.
The study was published in the journal eNeuro.