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Researchers May Have Found A Way To Reduce Brain Injury In Premature Babies

A recent study has identified the potential cause of brain injury in premature babies and provided a ray of hope to help diagnose it.

Statistics show that among 15 million infants born premature  before 37 weeks  approximately 9 million are left with lifelong brain injuries or damage. The good news is that researchers have spotted the underlying cause of such injuries and a way to tackle the so-called spur.

Microglia are immune cells that play a vital part in the baby's brain development process. However, if these cells suffer inflammation, they start to harm the infant's brain. This inflammation can be caused by several factors such as bacterial infection of the fetal membranes or maternal infection, or any other infection after the baby's delivery.

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After undergoing any such distortion, microglia cells damage the white matter, thereby reducing the degree to which neurons are insulated and impacting the connectivity to the brain. Researchers claim to have recognized the signaling pathway in these immune cells that leads to such a malignant transformation.

“We have actually identified the immune switch that turns these immune cells in the developing brain from being helpful in building a brain and taking care of the brain to causing damage,” said Dr. Bobbi Fleiss from RMIT University in Melbourne, Australia, a co-author of the study.

The study, which was conducted on mouse pups, experimented with the newly born pups which corresponded to 22 to 32 weeks of human pregnancy in terms of development. The pups were injected with proteins that resemble the same infection in the mother or fetus, which induces the change in microglia, converting it from a friend to an enemy. The team inferred that if they destroyed microglia selectively, it causes a significantly lower amount of destruction in the insulation of neurons. This is what led to the theory that overactive microglia causes brain injury.

With further research, they concluded that the pathway that includes microglia going into overdrive involves a gene named Wnt. This hypothesis was further tested out in a variety of animals as well as observed strictly in premature babies. The study in human tissue revealed that when inflammation was triggered, microglia became activated, and lower levels of molecules linked to the Wnt pathway were produced. The experimenters will continue to further research treatments based on their findings soon. “We think we are five to seven years away from this being a clinically applied therapy,” said Fleiss.

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Although premature delivery can't be predicted, and medication can't be provided to the pregnant mother, the infant can be treated immediately after birth. If these conclusions are solidified with further research, brain injuries in infants can be predicted at a very early stage, and they can undergo a low-risk remedy.

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