Abstract

It has been observed a correlation between tobacco consumption and a lower incidence of Parkinson’s disease (PD). The principal chemical compound found in tobacco is nicotine, which is a cholinergic agonist linked to cigarette addiction. Different studies have shown that there is a beneficial effect of nicotine on sporadic and genetic models of PD. In this work we evaluate the protective effect of nicotine in a Drosophila melanogaster model for PD by expression of Synphilin-1 (Sph-1) in dopaminergic neurons. Our results indicate that Sph-1 expression induces olfactory dysfunction one of the early phenotypes associated to PD. On the other hand, nicotine has a moderate effect on dopaminergic neuron survival that becomes stronger in older flies. Nicotine treatment also has beneficial effects on fly survival and motility, while maintaining tyrosine hydroxylase and dopamine levels, suggesting that the cholinergic agonist supports metabolic functioning of the surviving dopaminergic neurons that express Sph-1. The Sph-1 expressing fly is a good model for the study of early-onset phenotypes related with dopamine dysfunction. Our data also supports the idea that nicotine is an interesting therapeutic molecule for future research on phenotypic modulators of the disease and the development of new treatments.