ArticleActa neuropathologica communications2020
P53 aggregation, interactions with tau, and impaired DNA damage response in Alzheimer's disease.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Disentangling the inverse relationship between cancer and Alzheimer's or Parkinson's disease: A systematic review on Mendelian randomization studies.Neurobiology of disease · 2025Pooled it
- Connexin 50 mediates disease-relevant alpha-synuclein oligomer propagation and neuroinflammation in neurodegenerative disease.iScience · 2026Article
- Patient cerebral organoids capture Alzheimer's disease proteomic biomarkers and drug targets.bioRxiv : the preprint server for biology · 2026Article
- Nuclear Lamina Dysfunction and DNA Damage as Drivers of Premature Senescence in a Human Müller Glial Cell Model of Spinocerebellar Ataxia Type 7.International journal of molecular sciences · 2026Article
- RNA acetylation modification ac4C: An emerging regulatory hub of RNA metabolism disruption in Alzheimer's disease.Molecular biology reports · 2026Review
- TP53/TAU axis regulates microtubule bundling to control alveolar stem cell-mediated regeneration.The Journal of clinical investigation · 2026Article
- Drosophila wing is a high-throughput and versatile screening tool for Tau-mediated disease mechanisms and drug discovery.Disease models & mechanisms · 2026Article
- Nucleolar aggregation of key neuropathological proteins in the postmortem neurodegenerative brain.Acta neuropathologica · 2025Article
- Association Between U-p53AZ Blood Biomarker and White Matter Microstructure in Early Alzheimer's Disease: A Cross-Sectional Study Using AlzoSure® Predict.Health science reports · 2025Article
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- Neurodegeneration rewires the tumor microenvironment via the neuro-immune-cancer axis.iScience · 2025Review
- Article
- Potential role of TNFRSF12A in linking glioblastoma and alzheimer's disease via shared tumour suppressor pathways.Scientific reports · 2025Article
- The many connections of UFMylation with Alzheimer's disease: a comprehensive review.Molecular neurodegeneration · 2025Review
- Novel strategies for targeting tau oligomers in neurodegenerative diseases.Journal of neurology · 2025Review
- Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.Cell death and differentiation · 2025Article
- Pathogenic oligomeric Tau alters neuronal RNA processes through the formation of nuclear heteromeric amyloids with RNA-binding protein Musashi1.Progress in neurobiology · 2025Article
- The Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders.Neuroscience bulletin · 2025Review
- Understanding retinal tau pathology through functional 2D and 3D iPSC-derived in vitro retinal models.Acta neuropathologica communications · 2025Article
- Brain-derived tau oligomer polymorphs: distinct aggregations, stability profiles, and biological activities.Communications biology · 2025Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor, p53, is critical for many important cellular functions involved in genome integrity, including cell cycle control, DNA damage response, and apoptosis. Disruption of p53 results in a wide range of disorders including cancer, metabolic diseases, and neurodegenerative diseases. Alzheimer's disease (AD) is a neurodegenerative disorder characterized by protein aggregates that contribute to disease pathology. Although p53 is known to aggregate, its propensity to aggregate in AD has never been assessed. Moreover, AD neuropathology includes lethal cell cycle re-entry, excessive DNA damage, and abnormal cell death which are all controlled by p53. Here, we show p53 forms oligomers and fibrils in human AD brain, but not control brain. p53 oligomers can also be detected in htau and P301L mouse models. Additionally, we demonstrate that p53 interacts with tau, specifically tau oligomers, in AD brain and can be recapitulated by in vitro exogenous tau oligomer treatment in C57BL/6 primary neurons. p53 oligomers also colocalize, potentially seeding, endogenous p53 in primary neurons. Lastly, we demonstrate that in the presence of DNA damage, phosphorylated p53 is mislocalized outside the nucleus and p53-mediated DNA damage responders are significantly decreased in AD brain. Control brain shows a healthy DNA damage response, indicating a loss of nuclear p53 function in AD may be due to p53 aggregation and/or interactions with tau oligomers. Given the critical role of p53 in cellular physiology, the disruption of this crucial transcription factor may set an irreversible course towards neurodegeneration in AD and potentially other tauopathies, warranting further investigation.
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Registered trials
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