Neuroinflammation during Parkinson’s disease: Key cells and molecules involved in it

Abstract

Parkinson’s disease (PD), an idiopathic neurodegenerative disorder, is characterized by dopaminergic neuronal degeneration in the substantia nigra pars compacta of brain. Recent findings suggest the multifactorial etiology of the disease. Neuroinflammation and infiltration of peripheral inflammatory cells, chemokines, and cytokines may have a crucial role in PD pathogenesis. During the onset of the disease acute inflammation sets in to prevent dopaminergic neuronal death, but as the disease progresses neuroinflammation becomes chronic and promotes neurodegeneration. Rampant release of proinflammatory cytokines (TNF-α and IFN-γ), infiltration of peripheral CD4 and CD8 lymphocytes and augmented rate of reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation act as key players in disease progression. These proinflammatory factors are released by astrocytes stimulated by neuron derived α-synuclein which in turn recruit and activate microglia. These activated microglia contribute hugely to the progressive neurodegeneration in PD. In this chapter, we have summarized and discussed the findings on the neuroinflammarotry status in PD patients emphasizing on the role of cells and molecules involved. In addition, we have also discussed the plausible therapeutic interventions that may prove to be beneficial to PD patients.