The in vitro and in vivo models of PD discussed above, being based on the assumption that they truly de­scribe the pathogenesis of PD, reveal that the cell death mechanism underlying PD pathogenesis is apoptosis. However, the term apoptosis in its restricted sense of a specific phenotype may not be applicable to cell death seen in PD. For the in vitro models, cells used in cell cul­ture experiments are not the cells that are actually affected in PD, so their cellular contexts are different, and this can affect the responses of the cells when a neurotoxin, for example 6-OHDA, is given. The animal models have more advantages, but they also have some limitations; the most important one being the fact that the life-spans of the ani­mals used in these studies and the life-spans of human beings are very different, and this difference stems from the differences in metabolic rates. This could, of course, affect the metabolism of the agents given to the animals when creating PD models and the patterns of dysfunction observed in cellular structures like ubiqutin/proteasome system or mitochondria. The picture becomes more com­plicated when intercellular interactions, which affect cell interior and be affected in response to intracellular changes, are considered.