The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index.
Glial reactions in Parkinson's disease
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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“Remarkably, reactive M1 microglia were found several years after MPTP exposure in humans and non-human primates exposed to MPTP, indicating a long-lasting reactive microgliosis.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [233]
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Metadata
- 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
- 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
- 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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