UC San Diego researchers found that the chromosomal microdeletion 22q11.2del significantly increases the risk of spina bifida, identifying the CRKL gene as a key factor. They also highlighted the role of folic acid in reducing the risk and severity of the disorder.
The study also underscores the potential role of a common food supplement in reducing the risk of spina bifida. The findings were recently published in the journalGleeson, Rady Professor in the Department of Neuroscience and director of neuroscience at Rady Children’s Institute for Genomic Medicine, is the senior author of the study. He explained that spina bifida, also known as meningomyelocele, affects one in every 3,000 newborns. Unfortunately, the causes are mostly unknown.
Co-authors on a paper in the journal Science reporting a link between a chromosomal microdeletion and spina bifida include Joseph Gleeson and Keng Ioi “Harry” Vong, both of the UC San Diego School of Medicine Department of Neurosciences and the Rady Children’s Institute for Genomic Medicine. Credit: UC San Diego Health Sciences
“This finding really got us excited because it meant that CRKL disruption might be sufficient for spina bifida,” said Vong, co-first author of the study. “We removed the mouse Crkl gene ourselves and confirmed that some of the mice developed neural tube defects, including spina bifida.” Most of the other genes in 22q11.2 deletion were subsequently excluded, he added.may modulate CRKL-mediated spina bifida.
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