Abstract
The etiology of autism, a complex neurodevelopmental disorder, remains largely unexplained. Here, we explore the role of CpG and CpH (H=A, C, or T) methylation within autism-affected cortical brain tissue. While no individual site of methylation was significantly associated with autism after multi-test correction, methylated CpH di-nucleotides were markedly enriched in autism-affected brains (~2-fold enrichment at p <0.05 cut-off, p=0.002). These results further implicate epigenetic alterations in pathobiological mechanisms that underlie autism.
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