@ARTICLE{10.3389/fncel.2015.00437, AUTHOR={Vieira, Bruno Di Marco and Radford, Rowan A. and Chung, Roger S. and Guillemin, Gilles J. and Pountney, Dean L.}, TITLE={Neuroinflammation in Multiple System Atrophy: Response to and Cause of α-Synuclein Aggregation}, JOURNAL={Frontiers in Cellular Neuroscience}, VOLUME={9}, YEAR={2015}, URL={https://www.frontiersin.org/articles/10.3389/fncel.2015.00437}, DOI={10.3389/fncel.2015.00437}, ISSN={1662-5102}, ABSTRACT={Multiple system atrophy (MSA) is a progressive neurodegenerative disease presenting with combinations of autonomic dysfunction, parkinsonism, cerebellar ataxia and/or pyramidal signs. Oligodendroglial cytoplasmic inclusions (GCIs) rich in α-synuclein (α-syn) constitute the disease hallmark, accompanied by neuronal loss and activation of glial cells which indicate neuroinflammation. Recent studies demonstrate that α-syn may be released from degenerating neurons to mediate formation of abnormal inclusion bodies and to induce neuroinflammation which, interestingly, might also favor the formation of intracellular α-syn aggregates as a consequence of cytokine release and the shift to a pro-inflammatory environment. Here, we critically review the relationships between α-syn and astrocytic and microglial activation in MSA to explore the potential of therapeutics which target neuroinflammation.} }