Deciphering variability in the role of interleukin-1 beta in Parkinson's disease

摘要

Although the role of inflammation in neurodegeneration has been well acknowledged, less is known on the issue of each cytokine in specific neurodegenerative diseases. In this review, we will present evidence elucidating that interleukin-1 beta (IL-1 beta) has a multi-faceted character in pathogenesis of Parkinson's disease, which is a progressive neurodegenerative disorder. Increased levels of IL-1 beta were found in PD patients. Besides, PD symptoms were observed in IL-1 beta wild-type, but not deficient, animals. These lines of evidence suggest that IL-1 beta may contribute to the initiation or progression of PD. On the other hand, some studies reported decreased levels of IL-1 beta in PD patients. Also, genetic studies provided evidence suggesting that IL-1 beta may protect individuals against PD. Presumably, the broad range of IL-1 beta role is due to its interaction with both upstream and downstream mediators. Differences in IL-1 beta levels could be because of glia population (i.e. microglia and astrocytes), mitogen-activated protein kinase and nuclear factor. light-chain-enhancer of activated B cells signaling pathways, and several mediators (including cyclooxygenase, neurotrophic factors, reactive oxygen species, caspases, heme oxygenase-1, and matrix metalloproteinases). Although far from practice at this point, unraveling theoretical therapeutic targets based on the up-down IL-1 beta neuroweb could facilitate the development of strategies that are likely to be used for pharmaceutical designs of anti-neurodegenerative drugs of the future.