ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Central and systemic endotoxin challenges exacerbate the local inflammatory response and increase neuronal death during chronic neurodegeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 380 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
380 citing papers in PubMed, 2 syntheses or guidelines pooled it, 769 citations in OpenAlex.
- Pooled it
- Is There an Association Between Parkinson's Disease and Periodontitis? A Systematic Review and Meta-Analysis.Journal of Parkinson's disease · 2023Pooled it
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- Epigenetic mechanisms of inflammatory memory in the central nervous system.Nature immunology · 2026Review
- The Oral-Brain Axis: Mechanistic Insights Linking Periodontitis With Alzheimer's and Parkinson's Diseases.Cureus · 2026Review
- Single-nucleus brain transcriptomics reveals microglia dysfunction in multiple system atrophy.Nature communications · 2026Article
- Systemic inflammation, delirium and clinical progression in mild-moderate Alzheimer disease.EBioMedicine · 2026Article
- Do microplastics play a role in the pathogenesis of neurodegenerative diseases? Shared pathophysiological pathways for Alzheimer's and Parkinson's disease.Molecular and cellular biochemistry · 2026Review
- Innate Immune Tolerance Regulates Microglia Response to Aβ Oligomers.Journal of neurochemistry · 2026Article
- Influenza A infection accelerates disease-associated microglia formation during physiological aging.bioRxiv : the preprint server for biology · 2025Article
- Acute neuroinflammation induces prolonged transcriptional reprogramming in microglia.Journal of neuroinflammation · 2025Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- Knockout of P2Y12 receptor facilitates neuronal envelopment by reactive microglia and accelerates prion disease.Journal of neuroinflammation · 2025Article
- Multi-omics machine learning classifier and blood transcriptomic signature of Parkinson's disease.Research square · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Ultrasound-Assisted HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Delirium pathophysiology in cancer: neurofilament light chain biomarker - narrative review.BMJ supportive & palliative care · 2025Review
- Knockout of P2Y12 receptor facilitates microglia-neuron body-to-body interactions and accelerates prion disease.bioRxiv : the preprint server for biology · 2025Article
- Impact of COVID-19 on functional, cognitive, neuropsychiatric, and health-related outcomes in patients with dementia: A systematic review.eNeurologicalSci · 2025Review
- Sex differences in the central and peripheral omega 3 oxylipin response to acute systemic inflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
320 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
5 authors.
Funding
Abstract
The contribution of inflammation to the progression of neurodegenerative diseases such as Alzheimer's, Parkinson's, and prion diseases is poorly understood. Brain inflammation in animal models of these diseases is dominated by chronic microglial activation with minimal proinflammatory cytokine expression. However, these inflammatory cells are "primed" to produce exaggerated inflammatory responses to subsequent lipopolysaccharide (LPS) challenges. We show that, using the ME7 model of prion disease, intracerebral challenge with LPS results in dramatic interleukin-1beta (IL-1beta) expression, neutrophil infiltration, and inducible nitric oxide synthase expression in the brain parenchyma of prion-diseased mice compared with the same challenge in normal mice. Systemic inflammation evoked by LPS also produced greater increases in proinflammatory cytokines, pentraxin 3, and inducible nitric oxide synthase transcription in prion-diseased mice than in control mice and induced microglial expression of IL-1beta. These systemic challenges also increased neuronal apoptosis in the brains of ME7 animals. Thus, both central and peripheral inflammation can exacerbate local brain inflammation and neuronal death. The finding that a single acute systemic inflammatory event can induce neuronal death in the CNS has implications for therapy in neurodegenerative diseases.
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What OpenQuestion holds
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.