Parkinson’s disease and enhanced inflammatory response

Abstract

Parkinson's disease (PD) is the first and second most prevalent motor and neurodegenerative disease, respectively. The clinical symptoms of PD result from a loss of midbrain dopaminergic (DA) neurons. However, the molecular cause of DA neuron loss remains elusive. Mounting evidence implicates enhanced inflammatory response in the development and progression of PD pathology. This review examines current research connecting PD and inflammatory response.

Role of the Transcription Factor Nrf2 in Parkinson’s Disease: New Insights

“…A link between inflammation and PD was first described in a postmortem study by McGeer et al in 1988, where activated microglia was found in the SN of PD patients [34]. Furthermore, several clinical studies have confirmed this association by reporting increased microglial activation and elevated pro-inflammatory cytokines in post-mortem brains and CSF [35][36][37] (Figure 2). These data have been also reproduced by experimental studies in animal models of the disease [23,38,39], where neuroinflammation has been shown to be an important contributor to PD progression.…”

“…These data have been also reproduced by experimental studies in animal models of the disease [23,38,39], where neuroinflammation has been shown to be an important contributor to PD progression. Moreover, preclinical PD models suggest that inflammation is a driving force in DA neuron loss [37]. This idea is supported by experiments where chronic intraperitoneal injection of bacterial lipopolysaccharide (LPS) elicits a systemic immune response and leads to DA neuron loss and PD pathology in mice [40,41].…”

Progressive loss of nigrostriatal dopaminergic neurons induced by inflammatory responses to fipronil

“…It is closely related to the initiation and progression of neuronal cell damage and plays a significant pathological role in the development of neurodegenerative diseases (Hunot et al, 1997;Slemmer et al, 2008;Stojkovska et al, 2015). During an inflammatory response in the brain, microglia become activated, releasing interleukin-1β (IL-1β), IL-6, IL-8, tumor necrosis factor-α (TNF-α), and superoxide.…”

Candidate genes for Parkinson disease: Lessons from pathogenesis

“…De- [118]. Inflammation was reported in several animal models of PD and, 579 conversely, the occurrence of PD-like neurodegeneration was found in 580 mouse models exposed to bacterial lipopolysaccharide (LPS) or viral 581 pathogens, suggesting that excessive inflammation may trigger neuro-582 nal loss [119,120]. Several PD-related proteins have been implicated in 583 the inflammatory response.…”