“Chinese Scientists Unveil Groundbreaking Autism Reversal Injection – A Game-Changer for Neurodevelopmental Disorders!”
Chinese scientists have achieved a groundbreaking advancement in medical science by developing the first injection capable of reversing symptoms of autism through genomic editing in mice. As reported by the South China Morning Post, researchers based in Shanghai have successfully tested this innovative treatment on mice, employing a genome editing system to modify the DNA of mice carrying a mutation associated with autism spectrum disorder (ASD) in certain individuals.
The results of the study, published in the journal Nature Neuroscience on November 27, revealed that mice receiving the injection with the editing system exhibited a reduction in behaviors linked to ASD. The researchers emphasized that the treatment method they discovered may not only be applicable to ASD patients but also to individuals with other genetic neurodevelopmental disorders.
Chinese scientists
ASD affects approximately 1% of the global population, with the US Centers for Disease Control and Prevention (CDC) reporting that one in every 36 children in the United States is diagnosed with this disorder. ASD can impede an individual’s ability to interact and communicate, leading to repetitive behaviors and intense interests.
In their investigation into the potential of genomic editing for treating ASD, the scientists focused on mutations in the MEF2C gene, which they identified as “strongly associated” with the disorder. The study, reported by the SCMP, suggested that mutations in this gene contribute to developmental deficits, speech difficulties, repetitive behaviors, and epilepsy.
According to Li Dali, a professor of Life Sciences at East China Normal University (not affiliated with the paper), this represents the first effective treatment of mice with ASD-related mutations using base editing in the brain, according to information from the Shenzhen-based autism media platform Dami & Xiaomi.
The treatment successfully restored MEF2C protein levels in various brain regions and reversed behavioral abnormalities in MEF2C-mutant mice, the paper reported. However, it was acknowledged that for some patients, the disorder may not be caused by a single nucleotide variation, as observed in the mice, but rather by more complex mutations that pose challenges for editing.
