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MLi-2 Kinase Inhibitor Fully Restores Neuronal Cilia and Promotes Recovery in a Parkinson’s Mouse Model

The preclinical success supports multiple ongoing LRRK2 inhibitor trials, suggesting that the approach could extend to non-genetic Parkinson’s.

Artist's impression of neurons in the brain.

Overview

  • Three months of dietary MLi-2 treatment reinstated primary cilia on striatal neurons and glial cells in LRRK2-mutant mice to levels seen in healthy controls
  • Cilia restoration reactivated Sonic Hedgehog signaling and normalized secretion of neuroprotective factors essential for neuron survival
  • Striatal dopamine nerve ending density doubled, marking measurable recovery of neurons that had been on a degenerative trajectory
  • Multiple clinical trials of LRRK2 inhibitors are currently under way to evaluate their safety and efficacy in Parkinson’s patients
  • Researchers plan to test the efficacy of MLi-2 in non-LRRK2 Parkinson’s disease models following these promising preclinical results