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Neuroinflammation in Parkinson’s disease: A target for neuroprotection?
Abstract
Parkinson's disease is characterised by a slow and progressive degeneration of dopaminergic neurons in the substantia nigra. Despite intensive research, the cause of the neuronal loss in Parkinson's disease is poorly understood. Neuroinflammatory mechanisms might contribute to the cascade of events leading to neuronal degeneration. In this Review, we describe the evidence for neuroinflammatory processes from post-mortem and in vivo studies in Parkinson's disease. We further identify the cellular and molecular events associated with neuroinflammation that are involved in the degeneration of dopaminergic neurons in animal models of the disease. Overall, available data support the importance of non-cell-autonomous pathological mechanisms in Parkinson's disease, which are mostly mediated by activated glial and peripheral immune cells. This cellular response to neurodegeneration triggers deleterious events (eg, oxidative stress and cytokine-receptor-mediated apoptosis), which might eventually lead to dopaminergic cell death and hence disease progression. Finally, we highlight possible therapeutic strategies (including immunomodulatory drugs and therapeutic immunisation) aimed at downregulating these inflammatory processes that might be important to slow the progression of Parkinson's disease.
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“Imaging sensitive to glial cells could be of large clinical importance in the future because glial cells are the targets of several emerging therapeutic strategies (Hirsch and Hunot, 2009;Wilbanks et al., 2019).”
From NODDI in clinical research (2020) · cites this paper as Hirsch and Hunot, 2009
In the citing paper
“Evidence in previous study pointed out that microglial cells medicated neuroinflammation triggered the cascade of inflammatory events leading to neuronal degeneration (Hirsch and Hunot, 2009; Bassani et al., 2015; Ye et al., 2018).”
From Mechanism of miR-132-3p Promoting Neuroinflammation and Dopaminergic Neurodegeneration in Parkinson’s Disease (2022) · cites this paper as Hirsch and Hunot, 2009
In the citing paper
“Neuroinflammation is regarded as an important pathophysiological feature of PD, which is associated with neurodegeneration [4].”
From Neuroprotective Effects of Sodium Butyrate by Restoring Gut Microbiota and Inhibiting TLR4 Signaling in Mice with MPTP-Induced Parkinson’s Disease (2023) · cites this paper as [4]
In the citing paper
“Elevated levels of cytokines and prostaglandins have been detected in the cerebrospinal fluid and brains of PD patients where they may in turn activate the microglia, induce migration of microglia to SN, and release pro-inflammatory cytokines, as well as neurotoxic molecules capable of further exacerbating the disease [453,454,455,456].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [456]
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Metadata
- Authors
- Hirsch, E. C., & Hunot, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- ORCID
- Hunot, Stéphane
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 8
- Issue
- 4
- Pages
- 382-397
- ISSN
- 1474-4422 (ISSN-L)
- OpenAlex
- W2111464898
- Cited by
- 1,984
- References
- 181
- Citations by year
- 2026: 109 · 2025: 108 · 2024: 99 · 2023: 120 · 2022: 143 · 2021: 143 · 2020: 136 · 2019: 116 · 2018: 140 · 2017: 109 · 2016: 112 · 2015: 145 · 2014: 101 · 2013: 107 · 2012: 92
- FWCI
- 10.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- 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, neuroinflammation, neuroprotection, dopaminergic neuron loss, substantia nigra, glial activation, peripheral immune cells, oxidative stress, non-cell autonomous neurodegeneration, immunomodulators, Parkinson's disease model
- MeSH terms
- Animals, Anti-Inflammatory Agents, Dopamine, Humans, Immunization, Immunologic Factors, Inflammation, Nerve Degeneration, Neurons, Parkinson Disease, Neuroimmunomodulation, Cell Death, Neuroprotective Agents
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