The data reviewed here demonstrate a capacity for neuronal plasticity in the aged human brain, even when affected by neurodegenerative disorders. However, given their location and environment, these morphological changes may have beneficial or deleterious consequences. In Parkinson disease, the changes observed in the substantia nigra are likely involved in compensatory mechanisms that may delay the appearance of the clinical symptoms, where as the synaptic plasticity in the striatum may aggravate the behavioral disturbances. Finally, it is likely that such synaptic plasticity requires a highly differentiated set of trophic molecules during the evolution of the pathological process. Further knowledge of these molecules is needed, however, before their use can be envisaged as possible therapeutic agents aimed at correcting the behavioral deficits owing to the disease.