ArticleNucleic acids research2015
DNA polymerase β deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 137 citations in OpenAlex.
- Transcriptomics Meta-Analysis Reveals Phagosome and Innate Immune System Dysfunction as Potential Mechanisms in the Cortex of Alzheimer's Disease Mouse Strains.Journal of molecular neuroscience : MN · 2023Pooled it
- Neurodegenerative Disease Associated Pathways in the Brains of Triple Transgenic Alzheimer's Model Mice Are Reversed Following Two Weeks of Peripheral Administration of Fasudil.International journal of molecular sciences · 2023Pooled it
- Investigation of base excision repair gene variants in late-onset Alzheimer's disease.PloS one · 2019Trial
- Advances in Alzheimer's disease: mechanistic insights and therapeutic targets.Science China. Life sciences · 2026Review
- The senescence-inhibitory p53 isoform Δ133p53α: enhancing cancer immunotherapy and exploring novel therapeutic approaches for senescence-associated diseases.GeroScience · 2026Review
- Hypomorphic Protein Expression of DNA Polymerase Beta in PolβBiomolecules · 2026Article
- Shared molecular mechanisms in aging and neurodegenerative diseases: from mechanistic insights to therapeutic strategies.Frontiers in human neuroscience · 2026Review
- Central Role of Toll-like Receptor-9 Gene Function in Inflammation-Mediated Neuronal Plasticity: Implications for Long-Term Memory Development.Molecular neurobiology · 2025Review
- Telomeric DNA damage response mediates neurotoxicity of Aβ42 oligomers in Alzheimer's disease.The EMBO journal · 2025Article
- Δ133p53α-mediated inhibition of astrocyte senescence and neurotoxicity as a possible therapeutic approach for neurodegenerative diseases.Neuroscience · 2025Review
- Review
- Review
- Effect of Dietary Ketosis and Nicotinamide Riboside on Hippocampal Krebs Cycle Intermediates and Mitochondrial Energetics in a DNA Repair-Deficient 3xTg/POLβJournal of neurochemistry · 2025Article
- Beyond oxidative stress: Ferroptosis as a novel orchestrator in neurodegenerative disorders.Frontiers in immunology · 2025Review
- Are board games useful for people with dementia? A preliminary study for a non-pharmacological intervention.Frontiers in psychology · 2025Article
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- Dysregulation of energy metabolism in Alzheimer's disease.Journal of neurology · 2024Review
- Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.Nucleic acids research · 2024Article
- Exogenous and endogenous formaldehyde-induced DNA damage in the aging brain: mechanisms and implications for brain diseases.Cell biology and toxicology · 2024Review
- Roles of Sirtuins in Hearing Protection.Pharmaceuticals (Basel, Switzerland) · 2024Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 2 institutions in 2 countries.
Funding
Abstract
We explore the role of DNA damage processing in the progression of cognitive decline by creating a new mouse model. The new model is a cross of a common Alzheimer's disease (AD) mouse (3xTgAD), with a mouse that is heterozygous for the critical DNA base excision repair enzyme, DNA polymerase β. A reduction of this enzyme causes neurodegeneration and aggravates the AD features of the 3xTgAD mouse, inducing neuronal dysfunction, cell death and impairing memory and synaptic plasticity. Transcriptional profiling revealed remarkable similarities in gene expression alterations in brain tissue of human AD patients and 3xTg/Polβ(+/-) mice including abnormalities suggestive of impaired cellular bioenergetics. Our findings demonstrate that a modest decrement in base excision repair capacity can render the brain more vulnerable to AD-related molecular and cellular alterations.
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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.