The 'supermodel' concept that swept through the fashion world in recent years elevated a small group of catwalk stars to previously unknown celebrity status. Presumably Kate, Naomi and the rest all had the attributes required to succeed in the fashion shows of London, Paris, Milan and New York.

Models of a very different type have been important in our attempts to understand the aetiology of neurodegenerative disorders such as Parkinson's disease and to test the therapeutic potential of various natural and synthetic compounds. Analogous to the world of high fashion, every once in a while a supermodel is proclaimed in this arena — usually on the basis of a superior match between the characteristics of the disease in question and those of a new or improved animal model system. Probably the most widely known supermodel in the field of Parkinson's disease is based on the use of the pro-toxin, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This toxin induced an acute parkinsonian syndrome in humans that was virtually indistinguishable from the idiopathic disease. The use of MPTP and its metabolite 1-methyl-4-pyridium (MPP+) to create rodent and primate models of Parkinson's disease that inhibit mitochondrial respiration at complex 1 of the electron transport chain have undoubtedly led to a greater understanding of the disease itself. But there are some aspects of the human disease that are not typically reproduced in animal models induced by these toxins, including the development of fibrillar cytoplasmic inclusions (Lewy bodies) containing ubiquitin and α-synuclein. So is there room for a new supermodel of Parkinson's disease?

A recent study by Betarbet, Sherer and colleagues indicates a possible candidate for supermodel status — administration of the pesticide rotenone (a complex 1 inhibitor) to rats. Continuous infusion of 2–3 mg per kg per day of rotenone via a jugular cannula for 1–5 weeks produced a highly selective degeneration of dopamine neurons of the nigrostriatal system and led to hypokinesia and rigidity. Moreover, the damaged nigral neurons accumulated fibrillar cytoplasmic inclusions that contained ubiquitin and α-synuclein, and may resemble those seen in Parkinson's disease.

For the authors, these results indicate that chronic exposure to a common pesticide may reproduce the anatomical, behavioural and neuropathological features of Parkinson's disease; for the field they may indicate even more — the birth of a new supermodel. Whereas the exact status of this model requires further research, epidemiological data indicating that pesticide exposure may be associated with an increased risk of developing Parkinson's disease will surely provide the impetus.