The motor symptoms of Parkinson’s disease are due to the progressive degeneration of dopaminergic neurons in the substantia nigra. Multiple neuroinflammatory processes are exacerbated in Parkinson’s disease, including glialmediated reactions, increased expression of proinflammatory substances, and lymphocytic infiltration, particularly in the substantia nigra. Neuroinflammation is also implicated in the neurodegeneration and consequent behavioral symptoms of many Parkinson’s disease animal models, although it is not clear whether these features emulate pathogenic steps in the genuine disorder or if some inflammatory features provide protective stress responses. Here, we compare and summarize findings on neuroinflammatory responses and effects on behavior in a wide range of toxin-based, inflammatory and genetic Parkinson’s disease animal models.
CITATION STYLE
Cebrián, C., Loike, J. D., & Sulzer, D. (2014). Neuroinflammation in parkinson’s disease animal models: A cell stress response or a step in neurodegeneration? Current Topics in Behavioral Neurosciences, 22, 237–270. https://doi.org/10.1007/7854_2014_356
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