ArticleJournal of neuroinflammation2019
Loss of NF-κB p50 function synergistically augments microglial priming in the middle-aged brain.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025Review
- The regulation of NFKB1 on CD200R1 expression and their potential roles in Parkinson's disease.Journal of neuroinflammation · 2024Article
- Article
- Fetal hypoxia results in sex- and cell type-specific alterations in neonatal transcription in rat oligodendrocyte precursor cells, microglia, neurons, and oligodendrocytes.Cell & bioscience · 2023Article
- The Pro-Inflammatory Deletion Allele of the NF-κB1 Polymorphism Is Characterized by a Depletion of Subunit p50 in Sepsis.International journal of molecular sciences · 2022Article
- Fetal inflammation induces acute immune tolerance in the neonatal rat hippocampus.Journal of neuroinflammation · 2021Article
- Acute TBK1/IKK-ε Inhibition Enhances the Generation of Disease-Associated Microglia-Like Phenotype Upon Cortical Stab-Wound Injury.Frontiers in aging neuroscience · 2021Article
- Diesel exhaust impairs TREM2 to dysregulate neuroinflammation.Journal of neuroinflammation · 2020Article
- Role of RPTPβ/ζ in neuroinflammation and microglia-neuron communication.Scientific reports · 2020Article
- Reactive oxygen species (ROS) as pleiotropic physiological signalling agents.Nature reviews. Molecular cell biology · 2020Review
- Nuclear Factor κB (NF-κB)-Mediated Inflammation in Multiple Sclerosis.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWhile NF-κB p50 function is impaired in central nervous system disease, aging in non-CNS tissues, and response to reactive oxygen species, the role of NF-κB p50 in aging-associated microglial pro-inflammatory priming is poorly understood.
methodsMale NF-κB p50
resultsPeripheral LPS injection in 9-month-old C57BL/6 mice resulted in lower NF-κB p50 DNA binding of nuclear extracts from the whole brain, when compared to 3-week-old C57BL/6 mice, revealing differences in LPS-induced NF-κB p50 activity in the brain across the mouse lifespan. To examine the consequences of loss NF-κB p50 function with aging, NF-κB p50
conclusionsThese findings support that loss of NF-κB p50 function and aging in middle-aged mice may interact to excessively augment peripheral/microglial pro-inflammatory responses and point to a novel neuroinflammation signaling mechanism independent the NF-κB p50/p65 transcription factor in this process.
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Registered trials
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