Elucidating the role of SINE non-coding RNAs in amyloid beta pathology

Despite recent advances in our understanding of gene expression networks in Alzheimer's disease (AD), the molecular mechanisms of its pathogenesis still remain unclear. Previous studies have shown that mechanisms involving non protein-coding RNAs transcribed by Short Interspersed Nuclear Element (SINE) are key in maintaining transcriptional homeostasis in cells. RNAs from SINE B2 repeats in mouse and SINE Alu repeats in human, control gene expressions through binding and inhibition of RNA Polymerase II. Here, an integrative RNA genomics and bioinformatics approach is applied to investigate the connection between SINE RNAs, amyloid beta neuro-toxicity and dementia both in mouse models of AD and brains of AD patients. Our data shows that processing of SINE RNAs is abnormally increased in response to amyloid beta toxicity, and is connected with deregulation of gene expression during amyloid beta pathology and AD.

Authors

• Cheng, Yubo
• University of Lethbridge. Faculty of Arts and Science

• non-coding RNA
• Alzheimer's disease
• SINE RNAs
• amyloid beta neuro-toxicity
• gene expression deregulation
• Non-coding RNA -- Research
• Alzheimer's disease -- Research
• Amyloid beta-protein
• Transposons -- Research
• Mobile genetic elements
• Genetic transcription -- Regulation
• Dissertations, Academic

Identifier

hdl:10133/6096

OAI identifier oai:identifier

oai:opus.uleth.ca:10133/6096