There is growing evidence showing that inflammation-related peripheral processes may initiate or contribute to the progression of neurodegeneration48,49, and the above-mentioned observations support that generation of AT1-AA and ACE2-AA induced by dopaminergic degeneration, or by peripheral inflammatory processes, could disrupt BBB facilitating the access of deleterious compounds, the activated B cells, and perhaps autoantibodies to the CNS, contributing to PD progression. The gene discussed is AGTR1; the disease is Parkinson disease.