Epilepsy Drug Lamotrigine Shows Promising Results in Switching off Symptoms of Autism Spectrum Disorders

A new study about autism spectrum disorders discovered a drug that could switch off its symptoms.

Anticonvulsant Lamotrigine For Epilepsy Could Work For Symptoms of Autistic Spectrum Disorders

Autism spectrum disorder (ASD) is a complex developmental condition affecting an estimated 5.4 million adults and one in 44 children in the United States. The condition affects one perceives and socializes with others and is often accompanied by abnormalities like epilepsy or hyperactivity, according to Centers for Disease Control and Prevention.

Researchers from Germany's Hector Institute for Translational Brain Research discovered that lamotrigine - an anticonvulsant or antiepileptic drug could curb behavioral and social problems linked to ASD, NYPost reported.

The outlet noted that it's the closest thing yet to a potential cure for humans.

According to lead researcher and cellular biologist Moritz Mall, drug treatment in adulthood can alleviate brain cell dysfunction and thus counteract the behavioral abnormalities typical of autism. This occurs after the absence of MYT1L has already hindered brain development during the organism's developmental phase.

A new study from Rutgers examines the rising autism rates in New York City and the surrounding area. They studied Lamotrigine, which is marketed under the brand name Lamictal, a medication used to treat epilepsy and stabilize mood in patients with bipolar disorder and they found promising results.

Lamotrigine typically costs less than $3 per pill. It reverses the genetic mutation-induced changes in brain cells.

ALSO READ: Autistic People Think Quite Similar to Those Without Autism, New Study Suggests

How Lamotrigine Works on ASD Symptoms

Scientists are searching diligently for the molecular abnormalities contributing to ASD. Autism has been linked to a large number of genetic factors that affect the molecular programs of nerve cells.

Mall of the Hector Institute for Translational Brain Research (HITBR) has conducted extensive research on the role of the MYT1L protein in various neuronal diseases. The protein is a transcription factor that helps determine which genes in a cell are active and which are not. Almost all nerve cells in the body produce MYT1L for the duration of their existence.

Mall had previously demonstrated that MYT1L protects the identity of nerve cells by inhibiting other developmental pathways that program a cell to become, for example, muscle or connective tissue. Several neurological diseases, such as schizophrenia and epilepsy, as well as brain malformations, have been linked to MYT1L mutations.

Mall and his team examined the functional relevance of the "guardian of neuronal identity" in the development of ASD in their current study, which is supported by the European Research Council (ERC). To accomplish this, they genetically silenced MYT1L in both mice and human nerve cells derived from laboratory-reprogrammed stem cells, according to SciTechDaily.

The absence of MYT1L led to electrophysiological hyperactivation in both mouse and human neurons, resulting in a reduction in nerve function. Lack of MYT1L caused brain abnormalities, such as a thinner cerebral cortex, in mice. In addition to social deficits and hyperactivity, the animals exhibited several ASS-typical behavioral changes.

What was truly noteworthy about the neurons lacking MYT1L was the fact that they produced an excess of sodium channels, which are normally restricted to heart muscle cells. These pore-shaped proteins allow sodium ions to pass through the cell membrane and are therefore essential for electrical conductivity and, by extension, cell function. When a nerve cell produces an excessive amount of these channel proteins, electrophysiological hyperactivation can occur.

Drugs that block sodium channels have been used extensively in clinical medicine. Among these is lamotrigine, which is intended to prevent epileptic seizures. When lamotrigine was administered to nerve cells lacking MYT1L, their electrophysiological activity returned to normal. Even ASD-related behaviors, such as hyperactivity, were suppressed in mice given the drug.

The new peer-reviewed study was published Tuesday in Molecular Psychiatry journal.