The premise that such functionally impaired neurons exist in PD is supported by post-mortem analysis described in the seminal paper of Kordower et al. [39], showing nearly complete loss of tyrosine hydroxylase reactivity in the dorsal putamen in patients with 4–5 years disease duration, whereas a small subpopulation of melanin-positive and tyrosine hydroxylase-positive substantia nigra pars compacta neurons usually remained [40]. Here, TH is linked to Parkinson disease.