Our observations of Parkinson-like deficits in our INCL model provided a rationale for assessing nigrostriatal DA involvement in these movement impairments of the Cln1−/− mouse by quantifying levels of TH in the substantia nigra as well as levels of DA, DOPAC, HVA, TH, and DAT in the corpus striatum. The gene discussed is PPT1; the disease is Parkinsonism.