LA JOLLA, CA September 1, 2011 Examining brain damage that occurs when fetuses in the womb are deprived of oxygen, researchers at The Scripps Research Institute have discovered that damage does not occur randomly but is linked to the specific action of a naturally occurring fatty molecule called LPA, acting through a receptor that transfers information into young brain cells.
This observation made in mice suggests that LPA may also be linked to the damage caused by oxygen deprivation in human fetuses. If that proves to be the case, the research may help scientists and physicians better understand and find new ways to address the numerous developmental disorders that can arise when fetuses are deprived of oxygen in the wombincluding mental retardation, epilepsy, schizophrenia, autism, cerebral palsy and a range of other physical and mental problems.
"Fetal brain damage from oxygen deprivation involves specific changes that are, surprisingly, mediated by this lipid signal called LPA," said Scripps Research Professor Jerold Chun, MD, PhD, a member of the Dorris Neuroscience Center who led the research, which appeared in an advance, online issue of the journal Proceedings of the National Academy of Sciences (PNAS) this week.
"Because this pathway can be targeted with drugs," he added, "the discovery suggests that creating new medicines that target LPA receptors may be a way of limiting or preventing serious developmental brain diseases."
Currently, there is no way to treat the neurological damage produced by oxygen deprivation.
How Lack of Oxygen Affects the Fetal Brain
A developing fetus might be temporarily deprived of oxygena condition known as "hypoxia"for any number of reasons, including disruption of blood flow, exposure to smoke, carbon monoxide, or physical trauma.
Physicians have long known that hypoxia can lead to brain damage and i
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Scripps Research Institute