An important feature of this AAV model is that a significant reduction in dopaminergic neurons is seen only 6 months post-transduction, but the overexpression of α-synuclein alone, even without the neurodegeneration, triggers microglial activation and neuroinflammation, as seen in PD, making it an ideal model to test therapeutics designed to target aggregated α-Syn [12,13]. The gene discussed is SNCA; the disease is Parkinson disease.