ArticleFree radical biology & medicine2009
Age-associated oxidative damage to the p62 promoter: implications for Alzheimer disease.
Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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
60 citing papers in PubMed, 104 citations in OpenAlex.
- Autophagy and selective autophagy receptors: Key players against Alzheimer's disease.Neural regeneration research · 2026Article
- Tau degradation in Alzheimer's disease: Mechanisms and therapeutic opportunities.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Involvement of Autophagic Machinery in Neuropathogenesis: Targeting and Relevant Methods of Detection.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Circ-Bptf Ameliorates Learning and Memory Impairments via the miR-138-5p/p62 Axis in APP/PS1 Mice.Molecular neurobiology · 2024Article
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- Comprehensive Overview of Alzheimer's Disease: Etiological Insights and Degradation Strategies.International journal of molecular sciences · 2024Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Increased Expression of Autophagy-Related Genes in Alzheimer's Disease-Type 2 Diabetes Mellitus Comorbidity Models in Cells.International journal of environmental research and public health · 2023Article
- Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression.International journal of molecular sciences · 2023Review
- Mechanistic insight into female predominance in Alzheimer's disease based on aberrant protein S-nitrosylation of C3.Science advances · 2022Article
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- Mapping the genetic landscape of early-onset Alzheimer's disease in a cohort of 36 families.Alzheimer's research & therapy · 2022Article
- Does Data-Independent Acquisition Data Contain Hidden Gems? A Case Study Related to Alzheimer's Disease.Journal of proteome research · 2022Article
- Genetic and Molecular Evaluation ofFrontiers in aging neuroscience · 2022Article
- Oxidative stress and visual system: a review.EXCLI journal · 2022Review
- Selective Autophagy Receptor p62/SQSTM1, a Pivotal Player in Stress and Aging.Frontiers in cell and developmental biology · 2022Review
- Macroautophagy and aging: The impact of cellular recycling on health and longevity.Molecular aspects of medicine · 2021Review
- Macroautophagy and Mitophagy in Neurodegenerative Disorders: Focus on Therapeutic Interventions.Biomedicines · 2021Review
- A neuropathological cell model derived from Niemann-Pick disease type C patient-specific iPSCs shows disruption of the p62/SQSTM1-KEAP1-NRF2 Axis and impaired formation of neuronal networks.Molecular genetics and metabolism reports · 2021Article
- The Links between Cardiovascular Diseases and Alzheimer's Disease.Current neuropharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The absence of the p62 gene in mouse brain leads to biochemical and cognitive deficits that resemble Alzheimer disease (AD). In this context, the objective of this study was to examine the relationship between age-induced oxidative damage to the p62 promoter and AD. Increased 8-OHdG staining, a marker of oxidative stress, was observed in brain sections from mice deficient in the p62 gene compared to control. Treatment of MEF cells deficient in p62 with H(2)O(2) resulted in decreased cell survival and an absence of Nrf2 nuclear translocation. The mouse p62 promoter exhibited elevated oxidative damage with increasing age, and the degree of p62 promoter damage was also age-correlated in human brain samples. In human subjects, the expression of p62 was decreased in AD brain relative to age-matched controls, and likewise decreased p62 expression correlated with oxidative damage to the promoter. Treatment of HEK cells with H(2)O(2) resulted in decreased p62 expression concomitant with increased promoter damage. Consistent with these findings, a transgenic AD mouse model also exhibited increased p62 promoter damage and reduced p62 levels in brain. Altogether, our results reveal that oxidative damage to the p62 promoter correlates with decreased expression of p62 and may contribute to age-associated neurodegenerative disease such as AD and others.
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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.