Behavioral improvement in MPtP-treated nonhuman primates in the HALLWAY task after transfer of tH cdnA to host astrocytes

Parkinson’s disease (PD) is a neurodegenerative and progressive pathology characterized by an imbalance in the basal ganglia circuit resulting from a large decrease in dopamine (DA) levels in the striatum. This decrease is caused by neuronal death in the substantia nigra (pars compacta). Clinically the syndrome is known as Parkinsonism, which is characterized by motor alterations such as rest tremor, rigidity to passive movements, difficulty in initiating movements, as well as slowness in voluntary movements (akinesia and bradikinesia). Other symptoms include postural alterations, loss of facial expression, gait and balance alterations. PD etiology is unknown, however, it has been reported that both genetic and environmental factors are involved (Fuente-Fernandez and Calne 2002, Le and Appel 2004). One of the most important models that reproduces the histological injuries, as well as behavioral, biochemical and cognitive alterations characteristic of idiopathic PD in both humans (Langston et al. 1983, Burns et al. 1985) and nonhuman primates (Burns et al. 1984, Langston et al. 1984, Di Paolo et al. 1986, Elsworth et al. 1989, Fernandez-Ruiz et al. 1995) is the administration of the mitochondrial complex I inhibitor 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This model has been used to evaluate different antiparkinsonian therapies including pharBehavioral improvement in MPtP-treated nonhuman primates in the HALLWAY task after transfer of tH cdnA to host astrocytes