Analysis of alternative splicing associated with aging and neurodegeneration in the human brain
Open accessAbstract
Age is the most important risk factor for neurodegeneration; however, the effects of aging and neurodegeneration on gene expression in the human brain have most often been studied separately. Here, we analyzed changes in transcript levels and alternative splicing in the temporal cortex of individuals of different ages who were cognitively normal, affected by frontotemporal lobar degeneration (FTLD), or affected by Alzheimer's disease (AD). We identified age-related splicing changes in cognitively normal individuals and found that these were present also in 95% of individuals with FTLD or AD, independent of their age. These changes were consistent with increased polypyrimidine tract binding protein (PTB)–dependent splicing activity. We also identified disease-specific splicing changes that were present in individuals with FTLD or AD, but not in cognitively normal individuals. These changes were consistent with the decreased neuro-oncological ventral antigen (NOVA)–dependent splicing regulation, and the decreased nuclear abundance of NOVA proteins. As expected, a dramatic down-regulation of neuronal genes was associated with disease, whereas a modest down-regulation of glial and neuronal genes was associated with aging. Whereas our data indicated that the age-related splicing changes are regulated independently of transcript-level changes, these two regulatory mechanisms affected expression of genes with similar functions, including metabolism and DNA repair. In conclusion, the alternative splicing changes identified in this study provide a new link between aging and neurodegeneration.
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RNA splicing deficits have previously been identified in AD brain and could impact transcription of many genes including tau, APP, and presenilins.
“We and others have previously identified RNA splicing deficits in AD brain which could have profound impact on transcription of many genes, including tau, APP, and presenilins (Bai et al., 2013; Tollervey et al., 2011).”
From A Multi-network Approach Identifies Protein-Specific Co-expression in Asymptomatic and Symptomatic Alzheimer’s Disease (2017) · cites this paper as Tollervey et al., 2011
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- Authors
- Tollervey, J. R., Wang, Z., Hortobágyi, T., Witten, J. T., Zarnack, K., Kayikci, M., Clark, T. A., Schweitzer, A. C., Rot, G., Curk, T., Zupan, B., Rogelj, B., Shaw, C. E., & Ule, J.
- Affiliations
- MRC Laboratory of Molecular Biology (GB)
- King's College London (GB)
- European Bioinformatics Institute (GB)
- Affymetrix (United States) (US)
- University of Ljubljana (SI)
- ORCID
- Venue
- Genome Research
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-08-16
- Volume
- 21
- Issue
- 10
- Pages
- 1572-1582
- ISSN
- 1088-9051 (ISSN-L)
- PMC
- PMC3202275
- OpenAlex
- W2065356080
- Cited by
- 252
- References
- 66
- Citations by year
- 2026: 13 · 2025: 20 · 2024: 15 · 2023: 23 · 2022: 17 · 2021: 20 · 2020: 17 · 2019: 16 · 2018: 13 · 2017: 19 · 2016: 16 · 2015: 18 · 2014: 13 · 2013: 14 · 2012: 17
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genome Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Repository of the University of Ljubljana (University of Ljubljana) (publishedVersion, other-oa)
- University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Wellcome Trust (089701, 089701/Z/09/Z)
- Javna Agencija za Raziskovalno Dejavnost RS (J2-2197, L2-1112, P2-0209, Z7-3665)
- Medical Research Council (MC_G1000733)
- FP7 Ideas: European Research Council (206726)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- alternative splicing, brain aging, neurodegeneration, frontotemporal lobar degeneration, Alzheimer's disease, temporal cortex, polypyrimidine tract-binding protein, nova, splicing regulation, transcriptome, neuronal gene expression, glial gene expression, DNA repair, metabolism
- MeSH terms
- Neuro-Oncological Ventral Antigen, Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Aging, Alzheimer Disease, Antigens, Neoplasm, Exons, Humans, Ion Channels, Middle Aged, Nerve Tissue Proteins, Synaptic Transmission, Temporal Lobe, Transcription, Genetic, Down-Regulation, Cell Adhesion Molecules, RNA-Binding Proteins, Alternative Splicing, Protein Isoforms, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Principal Component Analysis, Polypyrimidine Tract-Binding Protein, Young Adult, Frontotemporal Lobar Degeneration
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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