| Autor: |
Vieira BD; Menzies Health Institute Queensland, Griffith University Gold Coast, QLD, Australia., Radford RA; Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University Sydney, NSW, Australia., Chung RS; Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University Sydney, NSW, Australia., Guillemin GJ; Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University Sydney, NSW, Australia., Pountney DL; Menzies Health Institute Queensland, Griffith University Gold Coast, QLD, Australia. |
| Abstrakt: |
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. |
