Evidence of inflammatory system involvement in Parkinson's disease

Yinxia Chao, Siew Cheng Wong, Eng King Tan, Yinxia Chao, Siew Cheng Wong, Eng King Tan

Abstract

Parkinson's disease (PD) is a chronic neurodegenerative disease underpinned by both genetic and environmental etiologic factors. Recent findings suggest that inflammation may be a pathogenic factor in the onset and progression of both familial and sporadic PD. Understanding the precise role of inflammatory factors in PD will likely lead to understanding of how the disease arises. In vivo evidence for inflammation in PD includes dysregulated molecular mediators such as cytokines, complement system and its receptors, resident microglial activation, peripheral immune cells invasion, and altered composition and phenotype of peripheral immune cells. The growing awareness of these factors has prompted novel approaches to modulate the immune system, although it remains whether these approaches can be used in humans. Influences of ageing and differential exposure to environmental agents suggest potential host-pathogen specific pathophysiologic factors. There is a clear need for research to further unravel the pathophysiologic role of immunity in PD, with the potential of developing new therapeutic targets for this debilitating condition.

Figures

Figure 1
Figure 1
The paper is summarized in the schematic drawing. Genetic mutations and environmental exposures can selectively induce dopaminergic neuron loss in the SNc. The mechanism may involve both regional (microglia) and systematic (peripheral) immune dysregulation. The dysregulated immune system can either elicit or exacerbate dopaminergic neuron loss at SNc by direct contact or by overrelease of cytokines and other immune mediators and thus immune regulation may have great therapeutic potential in PD treatment.

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