Study may be first to prove that single gene controls human brain cell growth

Control of how rapidly neurons (nerve cells) in the brain proliferate (increase in number) is a fundamental feature of brain health and disease. It’s an important parameter of proper brain development. Abnormally rapid neuron proliferation is a feature of aggressive brain tumors. The work of McGill University scientists is showing, for the first time, impressive evidence that a single gene controls human brain cell growth.

It has been thought that the control of brain growth involves a vast and complex network of molecules and processes, although specifics about such a network have been more mysterious than not. Such a lack of knowledge interferes with identifying abnormal development or the presence of disease. It obscures points at which intervention in disease could be effective and obscures the type of interventions which potentially could be beneficial.

Carl Ernst, an associate professor in the Department of Psychiatry at McGill, and his team of researchers found that in patients with severe microcephaly there is loss of the FOXG1 gene in brain cells. Loss of the gene reduces brain cell proliferation. Using genetic engineering techniques, the scientists introduced and activated the FOXG1 in cells from a microcephaly patient. Different levels of activation showed corresponding increases in brain cell proliferation.  

This research indicates that a single gene could potentially be targeted to stop brain tumor cells from growing. Future gene therapy may involve this same gene to be activated in patients with microcephaly or other neurodevelopmental disorders.

Cluster of neuronal cells colored for genes known to be expressed in brain cells
Human neurons derived from urine allow students in the Ernst lab to model neurodevelopmental disease such as FOXG1 syndrome. This image shows a large cluster of neuronal cells that are colored for genes known to be expressed in brain cells. Once created, these neurons can be used to study developmental processes, test drugs, or genetically engineer changes to gene products that may be deficient in diseases such as FOXG1 syndrome. (Credit: Nuwan Hettige)

The study is published in the open access journal Stem Cell Reports.

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About the Author

Dr. Faith Coleman

Faith A. Coleman MD
Dr. Coleman is a graduate of the University of New Mexico School of Medicine and holds a BA in journalism from UNM. She completed her family practice residency at Wm. Beaumont Hospital, Troy and Royal Oak, MI, consistently ranked among the United States Top 100 Hospitals by US News and World Report. Dr. Coleman writes on health, medicine, family, and parenting for online information services and educational materials for health care providers.

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