ArticleAging and disease2018
The Synergy of Aging and LPS Exposure in a Mouse Model of Parkinson's Disease.
Article in Aging and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Pre-clinical Studies Identifying Molecular Pathways of Neuroinflammation in Parkinson's Disease: A Systematic Review.Frontiers in aging neuroscience · 2022Pooled it
- Investigating the efficacy, methods, and challenges of induced pluripotent stem cells (iPSC) therapy in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Early α-Synuclein Pathology Induces Neuroinflammation and Decreases Topoisomerase IIβ Expression in A53T Mice.Inflammation · 2025Article
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- C18:0 GM3 ganglioside's efficacy in LPS-induced parkinsonism: neuroprotection, inflammatory inhibition and gliosis mitigation.Behavioral and brain functions : BBF · 2025Article
- Therapeutic potential ofHeliyon · 2024Article
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- Primary cilia in Parkinson's disease: summative roles in signaling pathways, genes, defective mitochondrial function, and substantia nigra dopaminergic neurons.Frontiers in aging neuroscience · 2024Review
- Integrating Network Pharmacology, Transcriptomics to Reveal Neuroprotective of Curcumin Activate PI3K / AKT Pathway in Parkinson's Disease.Drug design, development and therapy · 2024Article
- Animal models of Parkinson's disease: bridging the gap between disease hallmarks and research questions.Translational neurodegeneration · 2023Review
- Aging, Parkinson's Disease, and Models: What Are the Challenges?Aging biology · 2023Article
- Effects of green tea polyphenols on inflammation and iron status.Journal of nutritional science · 2023Article
- Lipopolysaccharide mouse models for Parkinson's disease research: a critical appraisal.Neural regeneration research · 2022Review
- Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.Acta pharmacologica Sinica · 2022Review
- Histamine in the Crosstalk Between Innate Immune Cells and Neurons: Relevance for Brain Homeostasis and Disease.Current topics in behavioral neurosciences · 2022Review
- TLR2 and TLR4 in Parkinson's disease pathogenesis: the environment takes a toll on the gut.Translational neurodegeneration · 2021Review
- Comprehensive Perspectives on Experimental Models for Parkinson's Disease.Aging and disease · 2021Review
- Circadian Clock Regulates Inflammation and the Development of Neurodegeneration.Frontiers in cellular and infection microbiology · 2021Review
- Lipopolysaccharide animal models of Parkinson's disease: Recent progress and relevance to clinical disease.Brain, behavior, & immunity - health · 2020Review
- Contra-Directional Expression of Plasma Superoxide Dismutase with Lipoprotein Cholesterol and High-Sensitivity C-reactive Protein as Important Markers of Parkinson's Disease Severity.Frontiers in aging neuroscience · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is an inevitable physiological challenge occurring in organisms over time, and is also the most important risk factor of neurodegenerative diseases. In this study, we observed cellular and molecular changes of different age mice and LPS-induced Parkinson disease (PD) model. The results showed that behavioral performance and dopaminergic (DA) neurons were declined, accompanied by increased expression of pro-inflammatory factors (TLR2, p-NF-kB-p65, IL-1β and TNF-α), as well as pro-oxidative stress factor gp91phox in aged mice compared with young mice. Aging exaggerated inflammatory M1 microglia, and destroyed the balance between oxidation and anti-oxidation. The intranasal LPS instillation induced PD model in both young and aged mice. The poor behavioral performance and the loss of DA neurons as well as TLR2, p-NF-kB-p65, IL-1β, TNF-α, iNOS and gp91phox were further aggravated in LPS-aged mice. Interestingly, the expression of Nrf2 and HO-1 was up-regulated by LPS only in young LPS-PD mice, but not in aged mice. The results indicate that the synergy of aging process and LPS exposure may prominently aggravate the DA neurons loss caused by more serious neuroinflammation and oxidative stress in the brain.
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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.