Researchers at the Department of Science and Technology’s (DST) independent Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) have created a novel treatment that might assist people with autism or intellectual disabilities to live less reliant lives.

The majority of the current therapies used to treat intellectual impairment or autism spectrum disorder (ASD) focus on symptom relief. The phenotypes seen in neurodevelopmental diseases, particularly after brain development, are not corrected by these.

Researchers at JNCASR, lead by Tapas K. Kundu and James Clement, discovered a gene that is suppressed in the brains of autistic people in mouse research.

According to the study, “the acetylation of DNA-associated proteins, histones, or proteins that provide structural support for chromosomes is repressed in the brains of mice with mutated syngap gene, which is similar to humans with mutated syngap gene (present in autistic patients).” They said that KAT3B or p300 seems to be the epigenetic enzyme responsible for this acetylation.

Kundu’s team had already identified TTK21, an activator of this enzyme.

The researchers were able to cause acetylation in the brains of the Syngap1 autistic mice by conjugating this activator with glucose-derived nanosphere (CSP-TTK21) and feeding them.

According to study recently published in the journal Aging Cell, CSP-TTK21 was discovered to promote synaptic rearrangements and restore neuronal function, learning, and memory in Syngap1 mice, mostly when given after the brain is thought to be fully grown (in humans, teens).

According to the researchers, this study not only establishes a direct link between histone acetylation and autism for the first time, but it also offers a highly promising avenue for treating ASD.

By focusing on epigenetic changes in Syngap1-related intellectual disability (ASD), the research offers a novel treatment strategy that may help patients regain their deficiencies to the point where they may live less reliant on others.