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New Research Promises To Prevent Brain Damage In Premature Babies

Press release   •   Nov 06, 2019 08:10 EST

To Prevent Brain Damage In Premature Babies

Researchers from Stanford Burnham Prebys Medical Discovery Institute have unveiled a novel mechanism and potential molecular drug target that may protect premature newborns against brain disorder. Premature babies have delicate brain tissue that can be prone to bleeding and can end up in post-hemorrhagic hydrocephalus, which is a severe condition that causes excess fluid accumulation and brain dysfunction. Jerold Chun, the senior author of the study, says that in premature infants, the brain structure is extraordinarily fragile, and they hope that formulating a neuroprotective medicine will allow them to stop the brain condition from ever happening and give those infants a healthy life.

Nearly one in thousand babies develop hydrocephalus, a lifelong illness that happens due to the accumulation of excess cerebrospinal fluid in the brain. In premature babies, born before completion of 37 weeks of gestation, the condition often follows bleeding in the brain, termed as intraventricular haemorrhage. The only way to treat hydrocephalus is through brain surgery by placing a mechanical shunt that drains the extra fluid. Owing to recurrent infections and shunt failure, follow-up surgeries are usually needed as the child grows to adulthood. Based on the extent of the injury, cognitive, emotional, intellectual, and social development might be impaired, for which there exists no preventive or curative treatment. Shenandoah Robinson, M.D., Professor, Neurosurgery, Johns Hopkins Children’s Center, says that medical treatment to prevent hydrocephalus, commonly referred to as ‘water on the brain,’ in premature babies is an essential goal. The research builds upon another study that suggests that medical treatment for repairing motile cilia, which are the delicate fibers that release cerebrospinal fluid in the brain, can potentially spare the fragile newborns a lifetime of repetitive surgeries, and perhaps neurodevelopmental disabilities, adds Robinson.

With the new model, the team was able to observe that LPA acts via specific receptors, proteins on the surface of the brain cells, to disable cilia as well as kill the cells that extend the cilia, which disrupts the cerebrospinal fluid flow that is created by beating cilia, resulting in hydrocephalus. Chun says that with their improved model for hydrocephalus, which can discover what is encountered by premature infants, they hope to identify drug candidates for the treatment of hydrocephalus.

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