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

Article Type

Research Article

Publication Title

Gene Reports


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



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