LRRK2 activity amplification in RAB10 phosphorylation is most pronounced in professional phagocytes (microglia, macrophages) with high baseline LRRK2 expression and chronic cargo load. If neuroinflammatory LRRK2 activity in microglia is the primary driver of dopaminergic neuron loss, cell-type-targeted inhibition should outperform global LRRK2 blockade — while avoiding potential adverse effects from neuronal LRRK2 inhibition (lysosomal dysfunction, protein secretion impairment). Falsifiable prediction: Conditional LRRK2 knockout in Cx3cr1-Cre microglia should reduce dopaminergic neuron loss in PFF-injected mice by ≥30% more than Syn1-Cre neuronal LRRK2 KO (TH+ neuron count, ipsilateral SNc, 90d post-injection). pRAB10/RAB10 ratio in FACS-sorted microglia should show ≥5× higher LRRK2 activity than sorted neurons from the same brains at peak inflammation.