Cited by 1,984Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

Neuroinflammation in Parkinson’s disease: A target for neuroprotection?

Hirsch, Etienne C, Hunot, Stéphane·2009·The Lancet Neurology

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.

Integrity signals

Registry

Crossref · 10.1016/s1474-4422(09)70062-6

Cites

181 of 181 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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.

    “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

  • Neuroinflammation is an important pathophysiological feature of PD and is associated with neurodegeneration.

    “Neuroinflammation is regarded as an important pathophysiological feature of PD, which is associated with neurodegeneration [4].”
  • Elevated levels of cytokines and prostaglandins have been detected in the cerebrospinal fluid and brains of PD patients, where they may activate microglia, induce migration of microglia to SN, and release pro-inflammatory cytokines and neurotoxic molecules capable of exacerbating the disease.

    “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].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Hirsch, E. C., & Hunot, S.
Affiliations
Centre National de la Recherche Scientifique (FR)
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 › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review