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The Contribution of Microglia to Neuroinflammation in Parkinson's Disease
Katja Badanjak1, Sonja Fixemer1,2, Semra Smajić1
1Luxembourg Centre for Systems Biomedicine, University of Luxembourg, L-4367 Esch-sur-Alzette, Luxembourg.
Abstract:
With the world's population ageing, the incidence of Parkinson's disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.
Insights
Parkinson's disease (PD) involves a damaging cycle between neurons and microglia, driven by inflammation and cellular dysfunction. Understanding this microglia-neuronal interplay is key to developing new anti-inflammatory treatments for PD.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- The global population is aging, leading to an increased incidence of Parkinson's disease (PD).
- Inflammatory processes, particularly involving microglia, are increasingly recognized as central to PD pathology.
- Dysfunctional microglial phenotypes (impaired or overactivated) are observed in PD patients' brains.
Purpose of the Study:
- To review recent findings on the microglia-neuronal interplay in Parkinson's disease.
- To focus on human postmortem and single-cell studies, animal models, and iPSC-derived models.
- To explore emerging technologies and potential anti-inflammatory therapies for PD.
Main Methods:
- Review of human postmortem immunohistochemistry and single-cell studies.
- Analysis of findings from animal models and induced pluripotent stem cell (iPSC)-derived models.
- Integration of data from newly emerging technologies.
Main Results:
- Evidence suggests a vicious cycle between dying neurons and microglia contributes to PD progression.
- This cycle involves oxidative stress, impaired mitophagy/autophagy, alpha-synuclein accumulation, and pro-inflammatory cytokine release.
- Microglia play a critical, albeit complex, role in neuroprotection and neuroinflammation in PD.
Conclusions:
- Investigating the microglia-neuronal interaction is crucial for advancing Parkinson's disease research and treatment.
- Targeting inflammatory pathways involving microglia offers potential for novel anti-inflammatory therapies.
- Further research integrating human data, models, and new technologies is needed to combat PD.
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