The role of neuroinflammation on the pathogenesis of Parkinson's disease

• Published in: BMB reports Vol. 43; no. 4; pp. 225 - 232
• Main Authors: Chung, Y.C., Kyung Hee University, Seoul, Republic of Korea, Ko, H.W., Kyung Hee University, Seoul, Republic of Korea, Bok, E.G., Kyung Hee University, Seoul, Republic of Korea, Park, E.S., Kyung Hee University, Seoul, Republic of Korea, Huh, S.H., Kyung Hee University, Seoul, Republic of Korea, Nam, J.H., Kyung Hee University, Seoul, Republic of Korea, Jin, B.K., Kyung Hee University, Seoul, Republic of Korea
• Format: Journal Article
• Language: English
• Published: Korea (South) 생화학분자생물학회 01.04.2010
• Subjects: Animals; Astrocyte; Astrocytes - metabolism; BBB leakage; Blood-Brain Barrier - physiopathology; Disease Models, Animal; Encephalitis - complications; Encephalitis - immunology; Infiltration of peripheral immune cells; Inflammation Mediators - physiology; Mice; Microglia; Neuroglia - metabolism; Neurons - metabolism; Parkinson Disease - immunology; Parkinson Disease - therapy; Parkinson's disease; PATHOGENESE; PATHOGENESIS; PATOGENESIS; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2010.43.4.225

Parkinson's Disease (PD) is a common neurodegenerative disease characterized by the progressive degeneration of nigrostriatal dopaminergic (DA) neurons. Although the causative factors of PD remain elusive, many studies on PD animal models or humans suggest that glial activation along with neuroinflammatory processes contribute to the initiation or progression of PD. Additionally, several groups have proposed that dysfunction of the blood-brain barrier (BBB) combined with infiltration of peripheral immune cells play important roles in the degeneration of DA neurons. However, these neuroinflammatory events have only been investigated separately, and the issue of whether these phenomena are neuroprotective or neurotoxic remains controversial. We here review the current knowledge regarding the functions of these neuroinflammatory processes in the brain. Finally, we describe therapeutic strategies for the regulation of neuroinflammation with the goal of improving the symptoms of PD.