Exp Neurobiol 2016; 25(4): 147-155
Published online August 31, 2016
© The Korean Society for Brain and Neural Sciences
Eunju Leem1,2#, Kyoung Hoon Jeong1,2#, So-Yoon Won4, Won-Ho Shin5* and Sang Ryong Kim1,2,3,6*
1School of Life Sciences & Biotechnology, 2BK21 plus KNU Creative BioResearch Group, 3Institute of Life Science & Biotechnology, Kyungpook National University, Daegu 41566, 4Department of Biochemistry and Signaling Disorder Research Center, College of Medicine, Chungbuk National University, Cheongju 28644, 5Predictive Research Center, Korea Institute of Toxicology, Daejeon 34114, 6Brain Science and Engineering Institute, Kyungpook National University, Daegu 41944, Korea
Correspondence to: *To whom correspondence should be addressed.
Sang Ryong Kim, TEL: 82-53-950-7362, FAX: 82-53-943-2762
Won-Ho Shin, TEL: 82-42-610-8088, FAX: 82-42-610-8157
#These authors contributed equally to this work.
Although accumulating evidence suggests that microglia-mediated neuroinflammation may be crucial for the initiation and progression of Parkinson's disease (PD), and that the control of neuroinflammation may be a useful strategy for preventing the degeneration of nigrostriatal dopaminergic (DA) projections in the adult brain, it is still unclear what kinds of endogenous biomolecules initiate microglial activation, consequently resulting in neurodegeneration. Recently, we reported that the increase in the levels of prothrombin kringle-2 (pKr-2), which is a domain of prothrombin that is generated by active thrombin, can lead to disruption of the nigrostriatal DA projection. This disruption is mediated by neurotoxic inflammatory events
Keywords: Prothrombin kringle-2, Parkinson’s disease, Microglia, Toll-like receptor 4