The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Neuroinflammation in Parkinson’s Disease
Open accessAbstract
During the last two decades, a wealth of animal and human studies has implicated inflammation-derived oxidative stress and cytokine-dependent neurotoxicity in the progressive degeneration of the dopaminergic nigrostriatal pathway, the hallmark of Parkinson’s disease (PD). In this review, we discuss the various hypotheses regarding the role of microglia and other immune cells in PD pathogenesis and progression, the inflammatory mechanisms implicated in disease progression from pre-clinical and clinical studies, the recent evidence that systemic inflammation can trigger microglia activation in PD-relevant central nervous system regions, the synergism between gene products linked to parkinsonian phenotypes (α-synuclein, parkin, Nurr1, and regulator of G-protein signaling-10) and neuroinflammation in promoting neurodegeneration of the nigrostriatal pathway, and the latest update on meta-analysis of epidemiological studies on the risk-lowering effects of anti-inflammatory drug regimens.
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Citations
Cites
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
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Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
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“…was detectable in C57Bl/6 male mice 7 months after a single i.p. injection of high-dose LPS (5 mg/kg) in all likelihood mediated by circulating TNF (Qin et al., 2007), while female C57Bl/6 mice appeared to be more resistant and required repeated high-dose LPS injections to display the nigral…”
BackgroundFamilial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase
Shimura, H., Hattori, N., Kubo, S.-I., Mizuno, Y., Asakawa, S., Minoshima, S., Shimizu, N., Iwai, K., Chiba, T., Tanaka, K., et al. (2000) · Nature Genetics · doi:10.1038/77060 · Cited by 2,024 · cited 2×
“Although loss-of-function mutations in the E3 ligase Parkin give rise to a rare form or autosomal recessive parkinsonism (Shimura et al. 2000), mice deficient in 424 J Neuroimmune Pharmacol (2009) 4:419–429”
BackgroundMicroglial physiology: unique stimuli, specialized responses
Ransohoff, R. M., & Perry, V. H. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132528 · Cited by 1,858
Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism
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In vivo imaging of microglial activation with [11C](R)-PK11195 PET in idiopathic Parkinson's disease
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BackgroundOxidative stress and the pathogenesis of Parkinson's disease
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Cited by
Microglial Activation and Chronic Neurodegeneration
Lull, M. E., & Block, M. L. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2010.05.014 · Cited by 1,047
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Implications of glial nitric oxide in neurodegenerative diseases
Yuste, J. E., Tarragon, E., Campuzano, C. M., & Ros-Bernal, F. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00322 · Cited by 356
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Neuroinflammation in Parkinson's disease: role in neurodegeneration and tissue repair
Vivekanantham, S., Shah, S., Dewji, R., Dewji, A., Khatri, C., & Ologunde, R. (2015) · International Journal of Neuroscience · doi:10.3109/00207454.2014.982795 · Cited by 171
Metadata
- Authors
- Lee, J.-K., Tran, T., & Tansey, M. G.
- Venue
- Journal of Neuroimmune Pharmacology
- Published
- 2009-10-10
- Volume
- 4
- Issue
- 4
- Pages
- 419-429
- ISSN
- 1557-1890 (ISSN-L)
- 1557-1904
- OpenAlex
- W2076333673
- Cited by
- 171
- References
- 18
- FWCI
- 6.85
- Type
- journal article
- Language
- en
- Open access
- green
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