LRRK2 and Parkinson disease: These doubly constrained peptidespermeate cells, bind to both wild-type and PD-associated pathogenicforms of LRRK2, inhibit LRRK2 dimerization, downregulate LRRK2-mediatedkinase activity, inhibit LRRK2-mediated neuronal apoptosis, and donot induce mislocalization of LRRK2 to skein-like structures in cells.This study supports the hypothesis that the COR–COR dimer interfaceis critical for LRRK2 dimerization and provides an alternative strategyto LRRK2-targeted PD therapy.