In parallel experiments, using in vivo and in vitro PD models, we confirmed that these autoantibodies are associated with the neurodegenerative process and the accompanying neuroinflammatory changes, and led to further progression of neurodegeneration by increasing the activity of AT1 receptors and decreasing the activity of ACE2-related anti-inflammatory RAS axis, respectively. This evidence concerns the gene AGTR1 and Parkinson disease.