The DOI matches its Crossref record; 89 of the 89 references it cites were found in a registry or an index.
Neuroinflammation is a key player in Parkinson’s disease and a prime target for therapy
Open accessAbstract
Parkinson’s disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra and depletion of dopamine in the striatum, which lead to pathological and clinical abnormalities. Increasing evidence has demonstrated that inflammation is the fundamental process contributing to neuron death in PD. Neuroinflammation, which is characterized by activated microglia and infiltrating T cells at sites of neuronal injury, is a prominent contributor to the pathogenesis of progressive PD. Microglia play a critical role in forming a self-propelling cycle leading to sustained chronic neuroinflammation and driving the progressive neurodegeneration in PD. This activation depends heavily on the respiratory burst within the microglia, which in turn regulates a number of downstream pro-inflammatory activities. On the other hand, the adaptive immune responses, most notably T cells, are now emerging as important components of the inflammatory response that contribute to the pathogenesis of PD. This review paper focus on the understanding of the inflammatory etiology of PD, as well as the molecular signaling involved in this inflammatory response, with the aim to provide more effective treatments to slow down or halt the progression of chronic inflammation-induced CNS disorders, such as PD.
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Cites
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Interleukin-10 and the Interleukin-10 Receptor
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Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
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“Since it is known that systemically injected LPS cannot readily reach the brain, further studies show that pro-inflammatory factors, such as TNFa underlie the mechanism of systemic LPS-induced DA neurotoxicity (Qin et al. 2007).”
InfluentialSelf-citationNeuroinflammation in Parkinson’s disease: A target for neuroprotection?
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Microglia initiate central nervous system innate and adaptive immune responses through multiple TLRs
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Cited by
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Inflammation and white matter degeneration persist for years after a single traumatic brain injury
Johnson, V. E., Stewart, J. E., Begbie, F. D., Trojanowski, J. Q., Smith, D. H., & Stewart, W. (2013) · Brain · doi:10.1093/brain/aws322 · Cited by 1,045
Role of Oxidative Stress in Parkinson's Disease
Hwang, O. (2013) · Experimental Neurobiology · doi:10.5607/en.2013.22.1.11 · Cited by 835
Neuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts
Jellinger, K. A. (2012) · Movement Disorders · doi:10.1002/mds.23795 · Cited by 451
Role of microglia in CNS inflammation
Graeber, M. B., Li, W., & Rodriguez, M. L. (2011) · FEBS Letters · doi:10.1016/j.febslet.2011.08.033 · Cited by 392
“The concept of inflammation acting as a major factor in the pathogenesis of PD can be summarized as follows [28]: ‘‘Neuroinflammation, which is characterized by activated microglia and infiltrating T cells at sites of neuronal injury, is a prominent contributor to the pathogenesis of progressive PD.”
Background
Metadata
- Authors
- Qian, L., Flood, P. M., & Hong, J.-S.
- Venue
- Journal of Neural Transmission
- Published
- 2010-06-23
- Volume
- 117
- Issue
- 8
- Pages
- 971-979
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- OpenAlex
- W2072942101
- Cited by
- 287
- References
- 89
- FWCI
- 14.83
- Type
- journal article
- Language
- en
- Open access
- green
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- Qian, L., Flood, P. M., & Hong, J.-S. (2010). Neuroinflammation is a key player in Parkinson’s disease and a prime target for therapy. Journal of Neural Transmission. https://doi.org/10.1007/s00702-010-0428-1
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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