Amyloid precursor protein intra-cellular domain (AICD), A? and their confounding synergistic effects differentially regulate the degradome of cellular models of Alzheimer's disease

Altered expressions of protein-coding genes and microRNAs have been implicated in the pathogenesis Alzheimer's disease (AD). The disrupted miRNA landscape (degradome) has studied AD mainly from A? perspective. That Amyloid Precursor Protein C- terminal Domain (AICD) is involved altering cellular transcriptome reported, but its role degradome still unexplored. involvement other long non-coding RNAs (lncRNA) being realized recently. Using small RNA sequencing an cell model, we observed perturbations levels 47 miRNAs deregulated between control groups, 26 AICD + (AD) groups. Additionally, using a novel bioinformatics pipeline, obtained total 263 differentially expressed lncRNAs versus group, 41 group. Effect AICD, individually combination, were validated with top regulated hits. Several these found to target key Receptor Tyrosine Kinase (RTK) - many which are AD. Understanding context likely open up new putative targets for intervention.