Neonatal Brain Injuries Found Treatable Through Pre-Clinical Gene-Targeting Approach

A pre-clinical study discussed the contributing factors to preventing and recovering uncontrolled neonatal brain injuries.

The normal gestation phase involves a low oxygen supply for the development of the fetus. However, some preterm deliveries occur, resulting in an abrupt shift of the oxygen to high levels. During this scenario, the infant has been pushed to experience an intolerable condition that might risk its body functions, such as the brain organ.

Oxidative Stress, Cognitive Deficits, and Pregnancy

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When an intense change in the oxygen occurs, babies affected often require extensive breathing support due to the state of their immature lungs. The oxygen supply itself usually induces a separate problem when raised to extreme levels, causing unstable atoms called free radicals to form and eliminate corresponding cells of the child.

Premature babies contain undeveloped functions such as those under antioxidants that protect a body from cell damage. These undeveloped defenses might be disrupted and useless when exposed to a high oxygen environment.

Because of the lack of protection from oxidative stress, the antioxidants would not work against the damage brought to the brain regions of the infant. This severity is critically dangerous for the baby, as there are still no available solutions or even treatments for this type of brain injury up to this date.

Children's National Hospital experts recently conducted research that tells how oxidative stress modifies the glucose metabolism enzyme called GSK3β. Through this activity, the hippocampal interneuron development is altered and impairs a child's cognitive skills, such as learning and memory capabilities.

According to the research, the GSK3β located in the hippocampal interneurons could be inhibited and reverse the impacts posed by the cognitive and cellular problems from the injury.

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Gene-Targeting Solution for Neonatal Brain Injury

Children's National Research Institute director and District of Columbia Intellectual and Developmental Disabilities Research Center lead investigator Vittorio Gallo, who also served as author of the study, explained in a Medical Xpress report that their team was able to identify a defect in the particular cell population enveloped in the hippocampus and is responsible for the memory development.

The study was the first to specify the roles of oxidative stress and the like between GSK3β and hippocampus development in the neurodevelopmental disorders induced by oxidative stress as well as in other cognitive deficits.

The authors expect that their findings will be utilized for further studies regarding the development of potential methods to allow infants to recover from the dangers of neonatal brain injury.

Part of the investigation included a pre-clinical model of brain injury by inducing high oxygen levels. After specifying the cellular damage, the authors administered a gene-targeted approach that could reduce the GSK3β rates in the cells and interneurons involved. The experiment improved inhibitory neurotransmission, and a reversal of effects was observed over the oxidation-induced memory defects.

The study was published in JNeurosci, titled "Oxidative stress-induced damage to the developing hippocampus is mediated by GSK3beta."

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