According to a study, scientists can cure autism symptoms using Lamotrigine, a drug that is used to treat epilepsy and calm the mood in people with bipolar disorder and costs $3.
A $3 per pill epilepsy medication may be used to “turn off” the signs of autism in mice, according to researchers’ ground-breaking new research, which was just published in the peer-reviewed journal Molecular Psychiatry (pdf below).
A complicated developmental condition known as autism spectrum disorder affects how one in 44 children and an estimated 5.4 million (2.2%) individuals in the US see and interact with others. According to data from the Centers for Disease Control and Prevention, disorders like epilepsy or hyperactivity are frequently present alongside it.
Lamotrigine, an anti-seizure drug initially approved for use in the US in 1994, was discovered by a team of specialists at Germany’s Hector Institute for Translational Brain Research to be effective in reducing behavioural and social issues associated with the illness.
Their discoveries are currently being touted as the most promising human cure to date.
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“Apparently, drug treatment in adulthood can alleviate brain cell dysfunction and thus counteract the behavioral abnormalities typical of autism,” lead researcher and cellular biologist Moritz Mall said in a statement. “[This occurs] even after the absence of MYT1L has already impaired brain development during the developmental phase of the organism.”
Lamotrigine is a drug used to treat epilepsy and calm mood in people with bipolar disorder. It is marketed under the brand name Lamictal among other names.
The medication, which usually costs less than $3 a pill, functions by undoing modifications to brain cells brought on by a genetic mutation.
The MYT1L protein has been found as having a role in a number of neurological illnesses by scientists who have spent years carefully searching for the molecular abnormalities that lead to ASD.
Nearly all of the body’s nerve cells generate a protein known as a transcription factor, which determines which genes are or are not active in a cell. Additionally, by blocking other growth pathways that are programmed, it “protects the identity of nerve cells by suppressing other developmental pathways that program a cell towards muscle or connective tissue.”
The protein’s mutations have previously been connected to several neurological conditions and abnormalities of the brain.
Researchers at HITBR genetically “turned off” MYT1L in mice and human nerve cells to examine the protein’s effect on signs of autism. They discovered that this resulted in neuronal hyperactivation that impaired nerve function in mouse and human neurons.
The MYT1L-deficient mice had brain abnormalities and displayed a number of ASD-related behavioural alterations, such as hyperactivity or social impairments.
The discovery that the MYT1L-deficient neurons developed extra sodium channels, which are generally restricted to cells in the heart muscle, caused the most “striking” reaction, according to the researchers.
These proteins let sodium ions to pass through the cell membrane, which is essential for electrical conductivity and cell activity. Electrophysiological hyperactivation, a typical autistic sign, can be caused by nerve cells that overproduce these sodium channels.
“When MYT1L-deficient nerve cells were treated with lamotrigine, their electrophysiological activity returned to normal. In mice, the drug was even able to curb ASD-associated behaviors such as hyperactivity,” the statement continued.
These encouraging findings are timely given the sharp increase in autism incidence in the NYC metro area. From 1% of the population in 2000 to 3% in 2016, the New York-New Jersey metro area saw a threefold increase in autism diagnoses.
Since diagnoses of children without intellectual disabilities are less likely to have been made in the past, it is thought that some of the sharp rise in these diagnoses is caused by this.
According to a study published in the Lancet Psychiatry, researchers from doctors’ offices have doubled antipsychotic prescriptions to children and youth in England.
However, earlier, more precise diagnoses do not entirely account for the increased trend, which was based on CDC estimates. Experts have cautioned that the growth may be partially due to the growing trend of women having children later in life.
While research on lamotrigine’s effect on MYT1L is presently limited to mice, the researchers noted that the results are encouraging and clinical human studies are currently being prepared.
Read the study given below: