Figure 1.

Epigentic regulation of intron retention during aging and AD pathogenesis.

Increased IR is observed during aging and in AD brain tissues. Retained introns are significantly shorter in length, have higher CG content and RNA polymerase II (Pol II) occupancy when compared to the spliced introns. DNA methylation can inhibit IR via recruitment of MeCP2 and its interacting spliceosome components. In AD brain tissues, aberrant IR can also be driven by genetic variants (SNPs) or by the insouble protein aggregation of splicesome components. AD: Alzheimer’s disease; IR: intron retention; MeCP2: methyl-CpG-binding protein 2.