ArticleNeurobiology of disease2019
Genetic suppression of IKK2/NF-κB in astrocytes inhibits neuroinflammation and reduces neuronal loss in the MPTP-Probenecid model of Parkinson's disease.
Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- Dual-Pathway Astrocyte Failure in Parkinson's Disease: Therapeutic Targeting of Nrf2/TFEB Suppression and cGAS-STING/Ferroptosis Activation.Molecular neurobiology · 2026Review
- Innate immune signaling and functions in astrocytes.Nature immunology · 2026Review
- Astrocytic dysfunction in Parkinson's disease pathogenesis: focusing on alpha-synuclein.Inflammopharmacology · 2026Review
- Alexander's Disease: Potential Drug Targets and Future Directions.Molecular neurobiology · 2025Review
- Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies.Biomedicines · 2025Review
- Parkinson's disease and metabolic disorders, understanding their shared co-morbidity through the autonomic nervous system.Advances in genetics · 2025Review
- Role and mechanism of molecular hydrogen in the treatment of Parkinson's diseases.Frontiers in neuroscience · 2025Review
- Research progress on the role of exercise-regulated reactive astrocytes in the prevention and treatment of Parkinson's disease.Frontiers in aging neuroscience · 2025Review
- Gut to brain: essential micronutrient and trace element manganese transport, function and toxicity.Frontiers in physiology · 2025Review
- The impact of astrocytic NF-κB on healthy and Alzheimer's disease brains.Scientific reports · 2024Article
- Article
- LAR Downregulation Protects the Astrocytic U251 and Cocultured SH-SY5Y Cells in a Rotenone-Induced Parkinson's Disease Cell Model.International journal of molecular sciences · 2023Article
- The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?International journal of molecular sciences · 2023Review
- Helicobacter pylori outer membrane vesicles induce astrocyte reactivity through nuclear factor-κappa B activation and cause neuronal damage in vivo in a murine model.Journal of neuroinflammation · 2023Article
- Chronic delta-9-tetrahydrocannabinol (THC) treatment counteracts SIV-induced modulation of proinflammatory microRNA cargo in basal ganglia-derived extracellular vesicles.Journal of neuroinflammation · 2022Article
- Monocyte biomarkers define sargramostim treatment outcomes for Parkinson's disease.Clinical and translational medicine · 2022Article
- Astrocyte inflammatory signaling mediates α-synuclein aggregation and dopaminergic neuronal loss following viral encephalitis.Experimental neurology · 2021Article
- Neuroprotective Effect of Kinase Inhibition in Ischemic Factor Modeling In Vitro.International journal of molecular sciences · 2021Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Neuroinflammatory activation of glia is considered a pathological hallmark of Parkinson's disease (PD) and is seen in both human PD patients and in animal models of PD; however, the relative contributions of these cell types, especially astrocytes, to the progression of disease is not fully understood. The transcription factor, nuclear factor kappa B (NFκB), is an important regulator of inflammatory gene expression in glia and is activated by multiple cellular stress signals through the kinase complex, IKK2. We sought to determine the role of NFκB in modulating inflammatory activation of astrocytes in a model of PD by generating a conditional knockout mouse (hGfapcre/Ikbk2
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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.