My doctoral research delved into uncovering the molecular mechanisms of competing endogenous RNA regulators in Alzheimer's disease. Specifically, I aimed to understand how different endogenous non-coding RNA species compete with each other through microRNA response elements to regulate biological processes in the context of Alzheimer's disease. To accomplish this, I conducted transcriptomic sequencing of AD-model mice (APP/PS1 mouse model) and age-matched wildtype controls. As a result, I was able to construct the first long non-coding RNA/microRNA/mRNA competing endogenous RNA regulatory network in the APP/PS1 mouse model. The competing endogenous RNA network comprises four hub lncRNAs that compete with five seed microRNAs, which regulate 1082 downstream mRNAs significantly enriched in nine KEGG signaling pathways, such as actin cytoskeletal signaling. Through biochemical and cell biological approaches, I demonstrated that the long non-coding RNA Rpph1 upregulates CDC42 expression and promotes hippocampal neuron dendritic spine formation by competing with microRNA-330-5p. This work highlights cytoskeletal sprouting as a compensatory mechanism in AD pathology, which is closely related to my current postdoctoral research project. My research findings led to a first-author publication in Frontiers in Molecular Neuroscience in 2017, and a co-authored paper in Frontiers in Neuroscience in 2019. In a subsequent review article in Frontiers in Molecular Neuroscience in 2018, I proposed a competing endogenous RNA regulatory hierarchy hypothesis within the context of neurodegenerative disorders.