The relevance of dopaminergic function to Parkinson’s disease has been exploited for forty years, and pharmacological supplementation
of brain dopamine levels continues to be the primary goal of treatment. Novel pharmacotherapies are desperately needed to
attenuate disease progression, but a primary problem of research has been the daunting challenge of monitoring the degeneration
of dopamine neurons in a living organism. Enter C. elegans, a small nematode, complete with eight dopamine neurons, that is amenable to genetic manipulation and laboratory observation.
Through transgenic addition of the green fluorescent protein to the organism’s dopamine neurons, a model system has been developed
in which dopamine neurodegeneration, in vivo, can be assayed in a microtiter plate format. The induction of dopamine neuron
degeneration in these organisms results in the loss of green fluorescence—and the effect of gene products and chemical agents
upon such degeneration can be assessed on a high-throughput basis. The power of the model is just beginning to be tapped,
and the accuracy to which the model recapitulates the human disease is surprising. Today, novel targets for therapeutic intervention—and
potentially, novel drugs—promise to extend treatment beyond the brute aim of supplying degenerating neurons with dopamine.
