ABSTRACT
The previous chapters, from 16 to 22, have focused on the main available animal models of Parkinson’s disease (PD), describing its characteristics, reliability, and reproducibility, as well as the ability to produce quantifiable symptoms and pathophysiologic alterations that resemble human PD. It also described its many shortcomings, mostly arising from the fact of studying a different species and our lack of a complete understanding of the true pathophysiologic basis of the disease. Nevertheless, these models provide an opportunity to study potential therapies for PD, not only symptomatic, after the mostly dopaminergic degeneration has taken place but specially in the presymptomatic level, when disease onset can be “predicted” as opposed to human’s onset where it usually predates diagnosis and therefore recognition of pathology by many years. It should be recognized that this approach, although providing a better window to evaluate neuroprotection, has many flaws as we are unable to predict the time and means of neurodegeneration onset in humans at least at this point in time.
