ABSTRACT
In the late nineteenth century, neuroscientists began generating lesions in animals using surgical, thermal, electrolytic, and toxicant delivery approaches as a means for understanding the effects of central nervous system injury on brain function. In addition to correlating brain region with function, scientists using these lesioning approaches began to appreciate that these animal models displayed many behavioral similarities with known human neurological disorders and hence recognized their potential for offering insights into human disease mechanisms. Over the decades, novel strategies have been developed to generate new animal models with the hope that through such endeavors, new therapeutic modalities, as well as a better understanding of disease etiology, would emerge. Experience has shown that the demand for an animal model to replicate all neurological (i.e., behavioral, neurochemical, and neuropathological) features of the human condition may not be possible or necessary. Specically, although the overall utility of an animal model for a particular disease may be dependent on how closely it replicates the human condition, the value of a model may more readily rely on its ability to replicate specic key components, or may simply be due to its ease and practicality of use for addressing the scientic question(s) at hand. Together, a thorough understanding of the strengths of the different animal models of Parkinson’s disease (PD) can have the advantage of providing distinct but collectively important insights toward the disease itself.
