In a recent study, we have demonstrated that 12-month-old male A53T transgenic mice display several abnormalities reminiscent of human PD such as the following: (a) decreased immunoreactivity for tyrosine hydroxylase (TH) in the SNc and striatum; (b) increased levels of the neuroinflammatory markers ionized calcium-binding adaptor molecule 1 (IBA-1), in the striatum, and glial fibrillary acidic protein (GFAP), in the SNc and striatum; (c) motor deficits. Here, TH is linked to Parkinson disease.