Researchers of autism, have long suspected that there is not one autism, but rather there are many autisms - each with its underlying biology. All genetic research has a goal to understand all these undisclosed mechanisms and discovering new treatments based on the findings that they will get.
Prabhakar and Daniel Geschwind, of the David Geffen School of Medicine at the University of California, Los Angeles, who explored more about the cause of ASD. Their study focuses more of the likely role of histone acetylation in ASD. Recent research uncovers the role of histone acetylation and its other important processes which include regulating the structure and function of chromatin, in other words, the eukaryotic genome. Their analysis has focused on H3K27ac which is an excellent candidate to distinguish active from inactive enhancer elements according to Autism Speaks.
The results of Prabhakar and Geschwind study, suggests thatASD cases shared a common histone acetylation pattern at 5,000 gene loci which are approximately more than 68%, despite its wide range of genetic and environmental causes of ASD. By analyzing the BrainSpan, according to Science Daily, they found out that gene activation at or after birth near the first 12 months thatcorrelate with to the stage of neuronal maturation and synapse formation, which was indeed associated with the inflation of acetylation in the ASD brain.
Their study towards ASD, is the first comprehensive study, of how the chemical histone acetylation differs and it has made us see shared, all this amalgamate themes in what is often contemplated to be an amalgam of many diverse diseases rather than one single disease.
Though there are strengths and weaknesses about all these extensive studies about DNA Methylation in ASD. But despite their flaws, the recent studies of DNA methylation in ASD provide some useful insights into its ethology. There has been numbers of replicated, potential methylation biomarkers for ASD have emerged.
