ArticleFrontiers in molecular neuroscience2023
Alzheimer's disease pathogenetic progression is associated with changes in regulated retained introns and editing of circular RNAs.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Nusinersen: the antisense oligonucleotide at the forefront of spinal muscular atrophy treatment.RNA biology · 2026Review
- SpliceImpactR maps alternative RNA processing events driving protein functional diversity.Nucleic acids research · 2026Article
- Translation of circular RNAs.Nucleic acids research · 2025Review
- The Role of circRNAs in the Pathological Mechanisms of Alzheimer's Disease: Potential Biomarkers for Diagnosis.Current neuropharmacology · 2025Review
- Circular RNAs as disease modifiers of complex neurologic disorders.Frontiers in pharmacology · 2025Review
- Identification of pathological pathways centered on circRNA dysregulation in association with irreversible progression of Alzheimer's disease.Genome medicine · 2024Article
- Widespread transposable element dysregulation in human aging brains with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Investigation of the Circular Transcriptome in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2024Article
- Transcriptome- and proteome-wide effects of a circular RNA encompassing four early exons of the spinal muscular atrophy genes.Scientific reports · 2024Article
- Transcriptome- and proteome-wide effects of a circular RNA encompassing four early exons of the spinal muscular atrophy genes.Research square · 2024Article
- Analyzing alternative splicing in Alzheimer's disease postmortem brain: a cell-level perspective.Frontiers in molecular neuroscience · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
Introduction: The molecular changes leading to Alzheimer's disease (AD) progression are poorly understood. A decisive factor in the disease occurs when neurofibrillary tangles (NFT) composed of microtubule associated protein tau (MAPT) form in the entorhinal cortex and then spread throughout the brain. Methods: We therefore determined mRNA and circular RNA changes during AD progression, comparing Braak NFT stages I-VI. Total RNA was isolated from human brain (entorhinal and frontotemporal cortex). Poly(A)+ RNA was subjected to Nanopore sequencing, and total RNA was analyzed by standard Illumina sequencing. Circular RNAs were sequenced from RNase R treated and rRNA depleted total RNA. The sequences were analyzed using different bioinformatic tools, and expression constructs for circRNAs were analyzed in transfection experiments. Results: We detected 11,873 circRNAs of which 276 correlated with Braak NFT stages. Adenosine to inosine RNA editing increased about threefold in circRNAs during AD progression. Importantly, this correlation cannot be detected with mRNAs. CircMAN2A1 expression correlated with AD progression and transfection experiments indicated that RNA editing promoted its translation using start codons out of frame with linear mRNAs, which generates novel proteins. Discussion: Thus, we identified novel regulated retained introns that correlate with NFT Braak stages and provide evidence for a role of translated circRNAs in AD development.
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