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Microglial phagocytosis is enhanced by monomeric α‐synuclein, not aggregated α‐synuclein: Implications for Parkinson's disease
Author(s) -
Park JiYoung,
Paik Seung R.,
Jou Ilo,
Park Sang Myun
Publication year - 2008
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20691
Subject(s) - microglia , phagocytosis , parkinson's disease , biology , pathogenesis , alpha synuclein , neuroscience , microbiology and biotechnology , neuroimmunology , extracellular , neurodegeneration , chemotaxis , central nervous system , immunology , inflammation , disease , biochemistry , medicine , pathology , receptor
Gathering evidence has associated activation of microglia with the pathogenesis of numerous neurodegenerative diseases of the central nervous system (CNS) such as Alzheimer's disease and Parkinson's disease. Microglia are the resident macrophages of the CNS whose functions include chemotaxis, phagocytosis, and secretion of a variety of cytokines and proteases. In this study, we examined the possibility that α‐synuclein (α‐syn), which is associated with the pathogenesis of Parkinson's disease, may affect the phagocytic function of microglia. We found that extracellular monomeric α‐syn enhanced microglial phagocytosis in both a dose‐ and time‐dependent manner, but β‐ and γ‐ syn did not. We also found that the N‐terminal and NAC region of α‐syn, especially the NAC region, might be responsible for the effect of α‐syn on microglial phagocytosis. In contrast to monomeric α‐syn, aggregated α‐syn actually inhibited microglial phagocytosis. The different effects of monomeric and aggregated α‐syn on phagocytosis might be related to their localization in cells. This study indicates that α‐syn can modulate the function of microglia and influence inflammatory changes such as those seen in neurodegenerative disorders. © 2008 Wiley‐Liss, Inc.