ArticleOxidative medicine and cellular longevity2021
MUTYH Actively Contributes to Microglial Activation and Impaired Neurogenesis in the Pathogenesis of Alzheimer's Disease.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- FAM134B-mediated ER-phagy degrades APP and suppresses Alzheimer's disease pathology.The EMBO journal · 2026Article
- Decoding unchanged transcriptome of Alzheimer's disease reveals an NCAM1 mRNA switch as a potential biomarker.iScience · 2026Article
- The silent saboteur: oxidative stress and the path to cognitive dysfunction.Neurodegenerative disease management · 2025Review
- Integrative bioinformatics and machine learning approaches reveal oxidative stress and glucose metabolism related genes as therapeutic targets and drug candidates in Alzheimer's disease.Frontiers in immunology · 2025Article
- The relationship between adult hippocampal neurogenesis and cognitive impairment in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Comprehensive analysis of genetic risk loci uncovers novel candidate genes and pathways in the comorbidity between depression and Alzheimer's disease.Translational psychiatry · 2024Article
- FSHing for DNA Damage: Key Features of MutY Detection of 8-Oxoguanine:Adenine Mismatches.Accounts of chemical research · 2024Review
- Exploring the Causal Relationship Between Telomere Biology and Alzheimer's Disease.Molecular neurobiology · 2023Review
- OGG1 aggravates renal ischemia-reperfusion injury by repressing PINK1-mediated mitophagy.Cell proliferation · 2023Article
- Dual Effects of miR-181b-2-3p/SOX21 Interaction on Microglia and Neural Stem Cells after Gamma Irradiation.Cells · 2023Article
- Exploring the interaction between T-cell antigen receptor-related genes and MAPT or ACHE using integrated bioinformatics analysis.Frontiers in neurology · 2023Article
- AI-DrugNet: A network-based deep learning model for drug repurposing and combination therapy in neurological disorders.Computational and structural biotechnology journal · 2023Article
- Analysis of gene expression profiles in Alzheimer's disease patients with different lifespan: A bioinformatics study focusing on the disease heterogeneity.Frontiers in aging neuroscience · 2023Article
- Corrigendum to "MUTYH Actively Contributes to Microglial Activation and Impaired Neurogenesis in the Pathogenesis of Alzheimer's Disease".Oxidative medicine and cellular longevity · 2023Article
- Loss of CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The two faces of DNA oxidation in genomic and functional mosaicism during aging in human neurons.Frontiers in aging · 2022Review
- OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022Review
- Akebia saponin D protects hippocampal neurogenesis from microglia-mediated inflammation and ameliorates depressive-like behaviors and cognitive impairment in mice through the PI3K-Akt pathway.Frontiers in pharmacology · 2022Article
- Impaired pathways of detoxification and risk of Alzheimer's disease: Differential gene expression studies via gene set expression analysis.Journal of Alzheimer's disease reportsArticle
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is a major risk factor for Alzheimer's disease (AD), which is characterized by brain atrophy, amyloid plaques, neurofibrillary tangles, and loss of neurons. 8-Oxoguanine, a major oxidatively generated nucleobase highly accumulated in the AD brain, is known to cause neurodegeneration. In mammalian cells, several enzymes play essential roles in minimizing the 8-oxoguanine accumulation in DNA. MUTYH with adenine DNA glycosylase activity excises adenine inserted opposite 8-oxoguanine in DNA. MUTYH is reported to actively contribute to the neurodegenerative process in Parkinson and Huntington diseases and some mouse models of neurodegenerative diseases by accelerating neuronal dysfunction and microgliosis under oxidative conditions; however, whether or not MUTYH is involved in AD pathogenesis remains unclear. In the present study, we examined the contribution of MUTYH to the AD pathogenesis. Using postmortem human brains, we showed that various types of
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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.