Neuroinflammation in Parkinson's disease and its potential as therapeutic target
Open accessAbstract
Parkinson's disease (PD), the second most common age-associated neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons and the presence of α-synuclein-containing aggregates in the substantia nigra pars compacta (SNpc). Chronic neuroinflammation is one of the hallmarks of PD pathophysiology. Post-mortem analyses of human PD patients and experimental animal studies indicate that activation of glial cells and increases in pro-inflammatory factor levels are common features of the PD brain. Chronic release of pro-inflammatory cytokines by activated astrocytes and microglia leads to the exacerbation of DA neuron degeneration in the SNpc. Besides, peripheral immune system is also implicated in the pathogenesis of PD. Infiltration and accumulation of immune cells from the periphery are detected in and around the affected brain regions of PD patients. Moreover, inflammatory processes have been suggested as promising interventional targets for PD and even other neurodegenerative diseases. A better understanding of the role of inflammation in PD will provide new insights into the pathological processes and help to establish effective therapeutic strategies. In this review, we will summarize recent progresses in the neuroimmune aspects of PD and highlight the potential therapeutic interventions targeting neuroinflammation.
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Inflammation is a significant contributor to Parkinson's disease neuropathology.
“While the etiology of PD is multifactorial, the role of inflammation has been deemed a significant contributor to neuropathology [3–5].”
From Intrastriatal injection of preformed alpha-synuclein fibrils alters central and peripheral immune cell profiles in non-transgenic mice (2019) · cites this paper as [5]
Reactive astrogliosis is characterized by increased expression levels of GFAP.
“Reactive astrogliosis is characterized by increased expression levels of GFAP [5].”
From Intrastriatal injection of preformed alpha-synuclein fibrils alters central and peripheral immune cell profiles in non-transgenic mice (2019) · cites this paper as [5]
Proinflammatory mediators TNF-α, IL-1β, and IFN-γ are found at higher levels in the midbrain of PD patients.
“In addition, proinflammatory mediators such as TNF-α, IL-1β, and IFN-γ have been found at higher levels in the midbrain of PD patients (Wang et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Wang et al., 2015
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- Authors
- Wang, Q., Liu, Y., & Zhou, J.
- Affiliations
- Chinese Academy of Sciences (CN)
- Corresponding author
- Zhou, Jiawei
- Venue
- Translational Neurodegeneration
- Published
- 2015-10-12
- Volume
- 4
- Issue
- 1
- Pages
- 19-19
- ISSN
- 2047-9158 (ISSN-L)
- PMC
- PMC4603346
- OpenAlex
- W2133712961
- Cited by
- 884
- References
- 125
- Citations by year
- 2026: 62 · 2025: 91 · 2024: 104 · 2023: 97 · 2022: 94 · 2021: 85 · 2020: 110 · 2019: 84 · 2018: 71 · 2017: 45 · 2016: 38 · 2015: 1
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Translational Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (CN) (31430036, 31123002, 31321091)
- Ministry of Science and Technology of the People's Republic of China (CN) (2011CB504102)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, neuroinflammation, dopaminergic neuron loss, substantia nigra pars compacta, alpha-synuclein aggregates, microglial activation, astrocytes, inflammatory cytokines, peripheral immune cells
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