On the one hand, neuronal alpha-synuclein produces an upregulation of AT1R while increasing in microglia the proportion of pro-inflammatory M1 versus neuroprotective M2 markers; accordingly, it is suggested that antagonists already used in hypertension and able to cross the blood-brain barrier may be repurposed for the therapy of PD [52]. This evidence concerns the gene AGTR1 and hypertensive disorder.