Researchers Noted a Reduction in ASD Behaviors When Using Lamotrigine on Genetically Altered Mice
Scientists from the Hector Institute of Translational Brain Research may have discovered a drug breakthrough with great potential for treating autism. This research was based on the hypothesis that autism could be associated with changes to the MYT1L protein, which normally protects the molecular identity of nerve cells. In the past, the MYT1L protein has been implicated in various neurodevelopmental disorders. The authors started their experiment by switching off the MYT1L protein in mice. When this happened, the mice exhibited brain abnormalities and displayed autism-like behavioral changes, such as social deficits and hyperactivity. The researchers then discovered that MYT1L-deficient neurons produced extra sodium channels in the mice that are typically restricted to cells in the heart muscle. These proteins are crucial for electrical conductivity and cell function and allow sodium ions to travel through the cell membrane. Nerve cells that over-generate these sodium channels can result in electrophysiological hyperactivation, which is often seen in autism. The next step for the research was to treat the mice with lamotrigine (brand name lamictal), a medication used to treat epilepsy and stabilize mood for people who have bipolar disorder. The authors saw behavioral improvements in the mice after they were treated with the drug. The researchers suggest these changes occurred after lamotrigine returned the mice’s electrophysiological activity to normal by treating their MYT1L-deficient nerve cells. Once this happened, the autism-associated behaviors were reduced, which delighted the study’s authors. It is important to note that this research is currently limited to mice. However, these results are extremely promising. Clinical human trials studying lamotrigine’s impact on MYT1L are currently being planned.
