Given the aforementioned problems with the current AAV-α-synuclein model, and the promising results reported from studies germane to the small molecule FN075, we sought to investigate if intra-nigral administration of AAV-α-synuclein followed by FN075 would enhance or precipitate α-synucleinopathy, nigrostriatal pathology and motor dysfunction in AAV-α-synuclein models of Parkinson’s disease. The gene discussed is SNCA; the disease is synucleinopathy.