A survey from 2012 of evidence for the role of neuroinflammation in neurotoxin animal models of Parkinson's disease and potential molecular targets

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Abstract

Parkinson's disease (PD) is a neurodegenerative movement disorder that results from the progressive loss of dopaminergic neurons in the midbrain substantia nigra pars compacta (SNpc). The specific molecular events that cause PD are currently not known; however, progress to better understand PD pathogenesis has been made using various animal models of the disease. In this review, we have highlighted reports from 2012 in which neurochemical/neurotoxins have been used in rodents to specifically address the role of neuroinflammation in the development and/or progression of PD-like pathology and in particular nigral degeneration. A number of studies have been summarized in which plausible pro-inflammatory, anti-inflammatory, or therapeutic agents targeting inflammatory pathways were introduced and/or investigated by various groups for neuroprotective effects. From these studies, it is clear that neuroinflammation acts to exacerbate the toxic outcomes that are set in motion within neurons following exposure to neurotoxins. Additionally, it is noted that future work is still needed to better understand the underlying mechanisms mediating the neuroinflammatory and neurotoxic phenotypes reported in rodent models of PD-like pathology to maximize the translation potential of these interventions to the clinic to prevent and/or delay PD onset and/or progression in humans.

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