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Greggio, E., Jain, S., Kingsbury, A., Bandopadhyay, R., Lewis, P., Kaganovich, A., van der Brug, M.P., Beilina, A., Blackinton, J., Thomas, K.J., Ahmad, R., Miller, D.W., Kesavapany, S., Singleton, A., Lees, A., Harvey, R.J., Harvey, K. and Cookson, M.R. (2006) Kinase Activity Is Required for the Toxic Effects of Mutant LRRK2/Dardarin. Neurobiology of Disease, 23, 329-341. http://dx.doi.org/10.1016/j.nbd.2006.04.001

has been cited by the following article:

• 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.