作者: George T. Kannarkat , Malú G. Tansey
DOI: 10.1007/978-3-319-08046-8_3
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摘要: Inflammation has recently been recognized as a significant feature of Parkinson’s disease (PD) pathophysiology, yet its role in limiting or promoting this neurodegenerative multisystem is not completely understood. Determining the inflammation PD will help understand how sporadic arises. Microglial activation, increased expression inflammatory genes, infiltration peripheral immune cells into central nervous system, and altered distributions make up vivo evidence for PD. Inflammatory hallmarks are also found animal models reviewed herein. Furthermore, we examine PD-linked genetic mutations may lead to function extent which these phenotypes recapitulated by environmental exposures that through similar mechanisms. Given implications involvement system on progression, conclude considering potential translation immunomodulatory therapies with demonstrated efficacy preclinical other immune-related conditions clinic. A clear need exists additional research innate adaptive immunity pathophysiology