The loss of neurons in the CNS as the result of degeneration or trauma following an accident does not initiate a process of self-repair. Though neuro-genesis takes place at low levels in the adult CNS, the loss of neurons in the above cases is definitive. In addition, in the situation of cell damage, when for instance processes of neurons are transected, neuronal connections cannot autonomically be repaired. The replacement of damaged or degenerated neurons with new ones that will integrate into the broken neuronal system or circuit was successfully undertaken in animals and so became a possibility for human beings too. Immature neurons appeared capable of integrating into the nervous system after implantation, which is not the case for adult neurons. Moreover, damaged neurons that do not restore their connections spontaneously, often maintain the intrinsic capacity to regenerate. Thus, the challenge is to find the conditions to evoke and guide regenerative fiber growth in the damaged brain.
The history of neurotransplantation goes back to 1890, when Thompson attempted to transplant neocortical brain tissue taken from a cat into the brain of dogs. His experiment largely failed, and it took until the 1970s for the work of Das and Altman (1971) and Bjorklund and Stenevi (1979) to show that only fetal neurons survived brain tissue grafting and that these cells are also able to reconstitute neural circuitry. Thereafter, the grafting of fetal nervous tissue was widely used in animal studies to investigate the processes of brain development. It was also applied as a possible repair strategy in a variety of animals to repair brain damage and neurological disorders.
Development towards a human application of these techniques accelerated after the observation of Perlow et al. in 1979 that grafting fetal nigral cells into the striatum of substantia nigra-lesioned rats reversed the motor disturbances. These rats were regarded as a partial model for Parkinson's disease since the gradual loss of dopaminergic neurons of the substantia nigra was seen as the origin of the movement disorders. Models of the disease were developed in primates that better represented the complexity of the disease in humans, with symptoms like tremor, rigidity and bradykinesia (Bjorklund 1992). Subsequent transplantation studies strongly validated the work undertaken in rats (Bakay et al. 1987; Fine et al. 1988; Bankiewicz et al. 1990). These results led to the first clinical studies in 1987, in which human fetal substantia nigra-containing tissue was placed in the dopamine-poor striatum of late stage PD patients (Lindvall et al. 1989; Madrazo et al. 1991). Hundreds of patients world-wide have received this experimental treatment since then. The first results were variable and were far from a complete and persistent recovery from the disease (e.g., Lindvall et al. 1989, Lindvall 1997; Madrazo et al. 1991; Olanow et al. 1996; Mehta et al. 1997).
The history of neural grafting in human PD can be seen as the test bed for neuron supplementation techniques as a therapeutic intervention in the human brain. It showed cell implantation deep inside the brain to be surgically feasible and proved that restorative neurosurgery using immature neurons is possible, at least in principle.
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