Cited by 701Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

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Glial reactions in Parkinson's disease

McGeer, Patrick L., McGeer, Edith G.·2008·Movement Disorders

DOI 10.1002/mds.21751

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Abstract

Dopaminergic neurons of the substantia nigra are particularly vulnerable to oxidative and inflammatory attack. Such processes may play a crucial role in the etiology of Parkinson disease (PD). Since glia are the main generators of these processes, the possibility that PD may be caused by glial dysfunction needs to be considered. This review concentrates on glial reactions in PD. Reactive astrocytes and reactive microglia are abundant in the substantia nigra (SN) of PD cases indicating a robust inflammatory state. Glia normally serve neuroprotective roles but, given adverse stimulation, they may contribute to damaging chronic inflammation. Microglia, the phagocytes of brain, may be the main contributors since they can produce large numbers of superoxide anions and other neurotoxins. Their toxicity towards dopaminergic neurons has been demonstrated in tissue culture and various animal models of PD. The MPTP and α‐synuclein models are of particular interest. Years after exposure to MPTP, inflammation has been observed in the SN. This has established that an acute insult to the SN can result in a sustained local inflammation. The α‐synuclein model indicates that an endogenous protein can induce inflammation, and, when overexpressed, can lead to autosomal dominant PD. Less is known about the role of astrocytes than microglia, but they are known to secrete both inflammatory and anti‐inflammatory molecules and may play a role in modulating microglial activity. Oligodendrocytes do not seem to play a role in promoting inflammation although, like neurons, they may be damaged by inflammatory processes. Further research concerning glial reactions in PD may lead to disease‐modifying therapeutic approaches. © 2007 Movement Disorder Society

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Authors: McGeer, P. L., & McGeer, E. G.
Affiliations: University of British Columbia (CA)
Corresponding author: McGeer, Patrick L.
ORCID: McGeer, Patrick L.
Venue: Movement Disorders
Publisher: Wiley
Published: 2007-11-28
Volume: 23
Issue: 4
Pages: 474-483
ISSN: 0885-3185 (ISSN-L)
1531-8257
DOI: 10.1002/mds.21751
OpenAlex: W2120412340
Cited by: 701
References: 106
Citations by year: 2026: 9 · 2025: 23 · 2024: 20 · 2023: 20 · 2022: 36 · 2021: 26 · 2020: 39 · 2019: 22 · 2018: 42 · 2017: 34 · 2016: 48 · 2015: 39 · 2014: 58 · 2013: 40 · 2012: 63
FWCI: 5.11
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Movement Disorders (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, glial reaction, reactive astrocytes, reactive microglia, substantia nigra, dopaminergic neurons, neuroinflammation, oxidative stress, MPTP, alpha-synuclein, oligodendrocytes, neuroprotection, disease-modifying therapy
MeSH terms: Animals, Haplorhini, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Brain, Dopamine, Female, HLA-DR Antigens, Humans, Immunohistochemistry, Inflammation, Male, Neurons, Neurotoxins, Parkinson Disease, Substantia Nigra, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Microglia, Oxidative Stress, Intercellular Adhesion Molecule-1, alpha-Synuclein

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