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Whole Transcriptome RNA-Seq Reveals Drivers of Pathological Dysfunction in a Transgenic Model of Alzheimer's Disease
Nikita Potemkin1,2, Sophie M F Cawood1,2,3, Diane Guévremont1,2
1Department of Anatomy, School of Biomedical Sciences, University of Otago, P.O. Box 56, Dunedin, New Zealand.
This study reveals a complex interplay of coding and non-coding RNA in Alzheimer's disease (AD) mouse models, driven by specific transcription factors. Findings highlight novel non-coding RNAs and their regulatory roles in AD pathogenesis.
Area of Science:
- Neuroscience
- Genomics
- Molecular Biology
Background:
- Alzheimer's disease (AD) affects millions globally, with incomplete understanding of its causes.
- Current research often focuses on protein-coding genes, potentially missing crucial regulatory elements.
- Non-coding RNAs (ncRNAs) and transcriptional regulators are increasingly recognized for their roles in complex diseases.
Purpose of the Study:
- To investigate comprehensive transcriptional changes in a murine model of Alzheimer's disease (APP/PS1 mice).
- To simultaneously analyze protein-coding genes and ncRNAs using whole transcriptome sampling.
- To identify key transcription factors regulating gene expression and ncRNA activity in AD.
Main Methods:
- Utilized whole transcriptome sampling in 15-month-old APP/PS1 mice.
- Performed gene expression profiling to identify differentially expressed genes and ncRNAs.
- Conducted transcription factor analysis and validated microRNA-mRNA interactions.
Main Results:
- Confirmed extensive involvement of microglia-associated genes and networks.
- Identified numerous differentially expressed ncRNAs, including microRNAs, long non-coding RNAs, and others.
- Determined six transcription factors regulating gene expression and eight transcription factors regulating miRNA expression.
Conclusions:
- A complex interplay between coding and non-coding RNAs contributes to transcriptional changes in AD.
- Specific transcription factors play a critical role in orchestrating these RNA-based regulatory networks.
- Findings offer new insights into AD biology and potential therapeutic targets.
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