RHOA and Alzheimer disease: Deletion of GTPase-activating proteins of RhoA can have opposing effects, suggesting tight regulation in neurons.86 Our data caution that a nuanced understanding of RhoA-ROCK inhibition is required before adoption as a PD therapeutic target.87,88 These data are reminiscent of AD and AD mouse models in which RhoA activity decreases with pathology progression, a phenomenon associated with neuritic dystrophy and RhoA sequestration within neurofibrillary tangles.89