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Published on: January 7, 2014
Glial reactions in Parkinson's disease
Patrick L McGeer1, Edith G McGeer
1Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada. mcgeerpl@interchange.ubc.ca
Movement Disorders : Official Journal of the Movement Disorder Society
|November 30, 2007
Summary
Parkinson disease (PD) may stem from glial dysfunction, as reactive microglia and astrocytes in the substantia nigra drive inflammation. Targeting these glial cells could offer new therapeutic strategies for PD.
Area of Science:
- Neuroscience
- Immunology
- Neuropathology
Background:
- Dopaminergic neurons in the substantia nigra are susceptible to oxidative and inflammatory damage, implicated in Parkinson disease (PD) etiology.
- Glial cells, particularly microglia and astrocytes, are key players in generating these damaging processes within the brain.
Purpose of the Study:
- To review the role of glial cell reactions in the pathogenesis of Parkinson disease.
- To explore how glial dysfunction contributes to the neuroinflammation observed in PD.
Main Methods:
- Review of literature focusing on glial responses in Parkinson disease.
- Examination of evidence from MPTP and alpha-synuclein models of PD.
- Analysis of the roles of microglia, astrocytes, and oligodendrocytes in PD-related inflammation.
Main Results:
- Reactive astrocytes and microglia are prevalent in the substantia nigra of PD patients, indicating significant neuroinflammation.
- Microglia can produce neurotoxins, contributing to dopaminergic neuron damage, as shown in experimental models.
- Both acute insults (MPTP) and endogenous proteins (alpha-synuclein) can trigger sustained inflammation in the substantia nigra.
Conclusions:
- Glial dysfunction is a critical factor to consider in Parkinson disease pathogenesis.
- Understanding glial reactions, especially microglial activity, may lead to novel disease-modifying therapies for PD.
- Astrocytes modulate inflammation, while oligodendrocytes appear less involved in promoting inflammation but are vulnerable to it.
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