Article citationsMore>>
Martin, I., Kim, J.W., Lee, B.D., Kang, H.C., Xu, J.C., Jia, H., Stankowski, J., Kim, M.S., Zhong, J., Kumar, M., Andrabi, S.A., Xiong, Y., Dickson, D.W., Wszolek, Z.K., Pandey, A., Dawson, T.M. and Dawson, V.L. (2014) Ribosomal Protein s15 Phosphorylation Mediates LRRK2 Neurodegeneration in Parkinson’s Disease. Cell, 157, 472-485.
http://dx.doi.org/10.1016/j.cell.2014.01.064
has been cited by the following article:
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TITLE:
LDN-73794 Attenuated LRRK2-Induced Degeneration in a Drosophila Parkinson’s Disease Model
AUTHORS:
Dejun Yang, Sharmila Das, Loujing Song, Tianxia Li, Jianqun Yan, Wanli W. Smith
KEYWORDS:
LRRK2, Parkinson’s Disease, LDN-73794, Kinase Activity, Neuronal Degeneration, Dopamine Neuron, Drosophila Model
JOURNAL NAME:
Advances in Parkinson's Disease,
Vol.4 No.3,
July
29,
2015
ABSTRACT: Parkinson’s disease (PD) is a common neurodegenerative disease with unclear pathogenesis. Currently, there are no disease-modifying neuron-protecting drugs to slow down the neuronal degeneration. Mutations in the leucine-rich repeat kinase 2 (LRRK2) cause genetic forms of PD and contribute to sporadic PD as well. Disruption of LRRK2 kinase functions has become one of the potential mechanisms underlying disease-linked mutation-induced neuronal degeneration. To further characterize the pharmacological effects of a reported LRRK2 kinase inhibitor, LDN-73794, in vitro cell models and a LRRK2 Drosophila PD model were used. LDN-73794 reduced LRRK2 kinase activity in vitro and in vivo. Moreover, LDN-73794 increased survival, improved locomotor activity, and suppressed DA neuron loss in LRRK2 transgenic flies. These results suggest that inhibition of LRRK2 kinase activity can be a potential therapeutic strategy for PD intervention and LDN-73794 could be a potential lead compound for developing neuroprotective therapeutics.
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