Neuropathological characterisation of the patient clusters at post mortem would help to address the question of the distribution and loads of α-synuclein, tau, vascular and amyloid pathology in driving both baseline clinical phenotype and subsequent motor and cognitive progression throughout the disease evolution of PD.27 It is intriguing to speculate whether patients in cluster 1, who have the fastest motor progression, prominent baseline non-motor symptoms, more symmetrical disease and a poor levodopa response, are defined by prominent cerebrovascular or amyloid pathologies. The gene discussed is MAPT; the disease is amyloidosis.