Neural transplantation as a therapy for neurodegenerative diseases has received much attention over the past two decades. The possibility that disease progress could be arrested and function restored raised hopes that a new treatment, particularly for Parkinson’s disease (PD), was imminent. Results with experimental models were promising, and, although clinical results have been mixed, there have been successes (see Lindvall, 1997, for a review). However, using fetal tissue as a source of neurons for transplantation in neurodegenerative diseases, such as PD or Huntington’s disease (HD), will always limit the acceptability and availability of this form of treatment. The ethical debate over the use of fetal tissue will not be resolved, and the practice of using this tissue is subject to the capriciousness of current public opinion and well-meaning government regulators. Furthermore, neuronal survival within the graft is often limited, necessitating the use of more tissue. In grafting studies in the hemiparkinsonian rat model, survival of dopaminergic neurons was estimated to be between 5–10% of the grafted dopaminergic (DA-ergic) neurons, based on the number of tyrosine hydroxylase (TH)-positive, immunohistochemically labeled neurons present in surviving grafts (Brundin and Bjorklund, 1987; Brundin et al., 1988). This number was compared to the number of immunostained DA-ergic neurons in the substantia nigra of adult mice, rats, and humans, as determined by (1983).