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Oxidative Medicine and Cellular Longevity
Volume 3 (2010), Issue 4, Pages 283-287

Alpha-Synuclein Stimulation of Astrocytes: Potential Role for Neuroinflammation and Neuroprotection

1Department of Anatomy, School of Medicine, Konkuk University, Seoul, Republic of Korea
2Department of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea
3IBST, Konkuk University, Seoul, Republic of Korea

Received 24 June 2010; Revised 26 June 2010; Accepted 29 June 2010

Copyright © 2010 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Selective loss of neurons, abnormal protein deposition and neuroinflammation are the common pathological features of neurodegenerative diseases, and these features are closely related to one another. In Parkinson's disease, abnormal aggregation and deposition of α-synuclein is known as a critical event in pathogenesis of the disease, as well as in other related neurodegenerative disorders, such as dementia with Lewy bodies and multiple system atrophy. Increasing evidence suggests that α-synuclein aggregates can activate glial cells to induce neuroinflammation. However, how an inflammatory microenvironment is established and maintained by this protein remains unknown. Findings from our recent study suggest that neuronal α-synuclein can be directly transferred to astrocytes through sequential exocytosis and endocytosis and induce inflammatory responses from astrocytes. Here we discuss potential roles of astrocytes in a cascade of events leading to α-synuclein-induced neuroinflammation.