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Extended LRRK2 Inhibition Reverses Parkinson’s Neuronal Damage in Mice

This approach marks the first reversal of early neuronal damage in genetic Parkinson’s models, pointing toward disease-modifying therapies.

Artist's impression of neurons in the brain.

Overview

  • Three-month daily administration of the MLi-2 LRRK2 kinase inhibitor fully restored primary cilia on striatal neurons and glia in LRRK2-mutant mice.
  • The treatment re-established Sonic Hedgehog–mediated neuroprotective signaling and doubled the density of dopamine nerve endings in the striatum.
  • Overactive LRRK2 disrupts primary cilia and neuronal communication, contributing to early Parkinson’s pathology in genetic cases.
  • Findings published in Science Signaling by Stanford University and University of Dundee researchers suggest functional improvement rather than mere symptom stabilization.
  • The research team plans to evaluate the inhibitor’s effects in non-LRRK2 Parkinson’s models and leverage ongoing human trials of LRRK2 inhibitors.