ArticleBMC medical genomics2019
Alternative cleavage and polyadenylation of genes associated with protein turnover and mitochondrial function are deregulated in Parkinson's, Alzheimer's and ALS disease.
Article in BMC medical genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Alternative Polyadenylation in the Brain is Modulated by Chronic Ethanol Exposure in a Sex- and Cell Type-Specific Manner.Molecular neurobiology · 2026Article
- Single-Cell Gene Module Inference Reveals Alternative Polyadenylation Dynamics Associated with Autism.International journal of molecular sciences · 2026Article
- Allele-specific alternative polyadenylation links noncoding genetic variation to Alzheimer's disease risk.bioRxiv : the preprint server for biology · 2026Article
- An Emerging Role for OGDHL: From Mitochondrial Energy Metabolism to Neurodevelopmental Disorders.Biology · 2025Review
- Decoding ALS from the tail end of RNA.Cell genomics · 2025Article
- Single-nucleus transcriptome atlas of orbitofrontal cortex in ALS with a deep learning-based decoding of alternative polyadenylation mechanisms.Cell genomics · 2025Article
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- RNA dysregulation in neurodegenerative diseases.The EMBO journal · 2025Review
- Comprehensive characterization of the transcriptional landscape in Alzheimer's disease (AD) brains.Science advances · 2025Article
- Exploring the Potential of CSTF1 as a Prognostic Biomarker in Hepatocellular Carcinoma and Its Correlation with Immune Infiltration.Journal of hepatocellular carcinoma · 2025Article
- Review
- PolyAMiner-Bulk is a deep learning-based algorithm that decodes alternative polyadenylation dynamics from bulk RNA-seq data.Cell reports methods · 2024Article
- Bovine C-X-C Motif Chemokine Ligand 14 Expression Is Regulated by Alternative Polyadenylation and MicroRNAs.Animals : an open access journal from MDPI · 2023Article
- Brain-Derived Neurotrophic Factor Dysregulation as an Essential Pathological Feature in Huntington's Disease: Mechanisms and Potential Therapeutics.Biomedicines · 2023Review
- Review
- Review
- Emerging roles of alternative cleavage and polyadenylation (APA) in human disease.Journal of cellular physiology · 2022Review
- RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis.International journal of molecular sciences · 2021Review
- RNA Dynamics in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Review
- TREND-DB-a transcriptome-wide atlas of the dynamic landscape of alternative polyadenylation.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTranscriptome wide changes have been assessed extensively during the progression of neurodegenerative diseases. Alternative polyadenylation (APA) occurs in over 70% of human protein coding genes and it has recently been recognised as a critical regulator of gene expression during disease. However, the effect of APA in the context of neurodegenerative diseases, to date, has not been widely investigated. Dynamic Analysis of Alternative Polyadenylation from RNA-seq (DaPars) is a method by Xia and colleagues [Nat Commun. 5:5274, 2014] to investigate APA using standard RNA-seq data. Here, we employed this method to interrogate APA using publicly available RNA-seq data from Alzheimer's disease (AD), Parkinson's disease (PD) and Amyotrophic Lateral Sclerosis (ALS) patients and matched healthy individuals.
resultsFor all three diseases, we found that APA profile changes were limited to a relative small number of genes suggesting that APA is not globally deregulated in neurodegenerative disease. However, for each disease phenotype we identified a subgroup of genes that showed disease-specific deregulation of APA. Whilst the affected genes differ between the RNA-seq datasets, in each cohort we identified an overrepresentation of genes that are associated with protein turnover pathways and mitochondrial function.
conclusionsOur findings, while drawn from a relatively small sample size, suggest that deregulation of APA may play a significant role in neurodegeneration by altering the expression of genes including UBR1 and OGDHL in AD, LONP1 in PD and UCHL1 in ALS. This report thus provides important novel insights into how APA can shape neurodegenerative disease characteristic transcriptomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.