Intron Retention and Alzheimer's Disease (AD): A Review of Regulation Genes Implicated in AD

Determining the genetic variations of candidate genes in affected subjects will help identify early pathological biomarkers of Alzheimer's disease (AD) and develop effective treatments. It has recently been found that some genes that are linked share an increase in intron retention (IR). In this review, we discuss a few instances of mRNA-IR in various genes linked to AD, including APOE, MAPT-Tau, Psen2, Farp1, Gpx4, Clu, HDAC4, Slc16a3, and App genes. These genes are vulnerable to IR, encompassing additional crucial proteins for brain functionality, but they are frequently involved in pathways linked to the control of mRNA and protein homeostasis. Despite the advancements in human in vivo RNA therapy, as far as we know, there are no reports of data generated regarding artificial in vivo splicing in either animal models or humans. To prevent genetic variations and improve or repair errors in expression of desired genes, humans have adopted new gene editing techniques like CRISPR-Cas9 and RNAi modalities. Ultimately, IR could be utilized as a therapeutic potential biomarker for disorders related to intronic expansion.