The DOI matches its Crossref record; 105 of the 106 references it cites were found in a registry or an index.
The lipopolysaccharide Parkinson’s disease animal model: mechanistic studies and drug discovery
Open accessAbstract
Research in the last two decades has unveiled an important role for neuroinflammation in the degeneration of the nigrostriatal dopaminergic (DA) pathway that constitutes the pathological basis of the prevailing movement disorder, Parkinson’s disease (PD). Neuroinflammation is characterized by the activation of brain glial cells, primarily microglia and astrocytes that release various soluble factors that include free radicals (reactive oxygen and nitrogen species), cytokines, and lipid metabolites. The majority of these glia‐derived factors are proinflammatory and neurotoxic and are particularly deleterious to oxidative damage‐vulnerable nigral DA neurons. As a proof of concept, various immunologic stimuli have been employed to directly induce glial activation to model DA neurodegeneration in PD. The bacterial endotoxin, lipopolysaccharide (LPS), has been the most extensively utilized glial activator for the induction of inflammatory DA neurodegeneration. In this review, we will summarize the various in vitro and in vivo LPS PD models. Furthermore, we will highlight the contribution of the LPS PD models to the mechanistic studies of PD pathogenesis and the search for neuroprotective agents for the treatment of PD.
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“Neuroinflammation is characterised by the activation of microglia and astrocytes [29].”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [29]
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Metadata
- Authors
- Dutta, G., Zhang, P., & Liu, B.
- Affiliations
- University of Florida (US)
- Corresponding author
- Liu, Bin
- ORCID
- Liu, Bin
- Venue
- Fundamental & Clinical Pharmacology
- Publisher
- Wiley
- Published
- 2008-09-21
- Volume
- 22
- Issue
- 5
- Pages
- 453-464
- ISSN
- 0767-3981 (ISSN-L)
- 1472-8206
- PMC
- PMC2632601
- OpenAlex
- W2057913943
- Cited by
- 235
- References
- 106
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 14 · 2023: 10 · 2022: 15 · 2021: 19 · 2020: 15 · 2019: 10 · 2018: 13 · 2017: 14 · 2016: 14 · 2015: 13 · 2014: 14 · 2013: 16 · 2012: 22
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Fundamental and Clinical Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Environmental Health Sciences (ES013265, R01ES013265)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, lipopolysaccharide, neuroinflammation, nigrostriatal pathway, dopaminergic neuron loss, microglial activation, astrocytes, glial activation, neuroprotection, drug discovery, oxidative stress, cytokines, Parkinson's disease model
- MeSH terms
- Animals, Antiparkinson Agents, Disease Models, Animal, Humans, Lipopolysaccharides, Parkinson Disease, Drug Discovery
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