Well - known old
The epilepsy drug was able to suppress neurofibromatosis in mice
Researchers from Washington University School of Medicine in St. Louis have found that lamotrigine, a well-known drug used against epilepsy and bipolar disorders, stops the growth of tumors in mice with neurofibromatosis of the first type.
Neurofibromatosis of the first type is called a genetically determined disease in which a patient develops benign tumors from the nerve membranes (neurofibromas). They are nodules ranging in size from 0.1 to several centimeters. Neurofibromas rarely degenerate into malignant tumors and are not considered life-threatening. But sometimes they cause serious medical problems, including limited movement and blindness, when neurofibroma presses on neighboring tissues. In addition to neurofibromas, the disease manifests itself in the form of light brown spots on the skin, sometimes in the form of brain and optic nerve tumors, bone deformities and cognitive abnormalities, such as autism, learning disabilities, hyperactivity and attention deficit hyperactivity disorder. The disease is caused by a mutation in the Nf1 gene on the seventeenth chromosome. Neurofibromatosis of the first type occurs in one out of 3,500 newborns.
Last year, David H. Gutmann of Washington University in St. Louis and Professor of neurology Michelle Monje of Stanford University School of Medicine discovered that light causes increased activity of neurons in the eyes of mice with a mutation in the Nf1 gene, which then causes the formation of tumors on the optic nerve. Now they have continued working together with Corina Anastasaki from Washington University in St. Louis and Professor of Dermatology Liu Le (Lu Q. Le) from the University of Texas.
Scientists compared neurons of mice with and without mutations of the Nf1 gene. Neurons of mice with tumor-causing Nf1 mutations generated electrical impulses more often than neurons of healthy mice. These overexcited neurons then released molecules that stimulated the growth of brain and nerve tumors. The researchers found that the increased excitability was the result of ion channel dysfunction, which altered the underlying electrical activity inside the neurons. They also studied mice with a special type of Nf1 mutation found in people with type I neurofibromatosis who do not develop brain or nerve tumors. Anastasaki found that the neurons of mice with this specific Nf1 mutation are not hyperexcited and do not form tumors.
Hyperexcitable neurons are also a sign of epilepsy, and lamotrigine, an epilepsy drug, affects the same ion channel that is disrupted in hyperexcitable Nf1 mutant neurons. The researchers gave lamotrigine to a group of mice with the Nf1 mutation who developed optic nerve tumors. Compared to the placebo mice, their tumors were smaller and no longer grew.
In addition to a new treatment for neurofibromatosis of the first type, the results also offer a new explanation for the cognitive symptoms of the disorder. "A mutation in the Nf1 gene changes the basic biology of a neuron,— says David Gutmann. — During development, neurons form first and tell the rest of the brain how to form. If you have a mutation affecting the behavior of neurons, it can change everything in how the brain adjusts during development. Perhaps this discovery could lead to new treatments for learning and cognitive problems in children with neurofibromatosis."
The study was published in the journal Nature Communications (Anastasaki et al., Neuronal hyperexcitability drives central and peripheral nervous system tumor progression in models of neurofibromatosis-1).
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