[
International Worm Meeting,
2013]
With increasing life expectancy, neurodegenerative diseases have becomeever more common and Alzheimer's disease (AD) the most reported one. AD is mainly characterized by the presence of senile plaques in the brain formed by toxic peptide amyloid-b (Ab). The current explanation for Ab toxicity in AD still remains controversial in view of the fact that the relationship between Ab species and Ab specific behavior has not been defined in vivo. Simple invertebrate models of neurodegenerative diseases offer experimental advantages for addressing basic cellular processes that are conserved among all animals. The diphenyl diselenide (DPDS), an organic selenium compound, is characterized by its potential antioxidant, anti-inflammatory, hepatic and neuroprotective. This study aims to determine the effects of chronic treatment with DPDS in the nematode C. elegans model of AD. The wildtype strain N2 and transgenic worms which expresses the Ab1-42 constitutively (CL2006) or inducible in the body wall muscles (CL4176) and it's control strain (CL802), inducible neuronal Ab expression (CL2355) and it's control strain (CL2120) were treated with DPDS in different concentrations since eggs to adulthood. Behavioral assays (paralysis, chemotaxisqu and egg laying) and the levels of reactive oxygen species were quantified in order to verify if this compound is able to modulate the toxicity of the peptide by its antioxidant ability. DPDS reduced the levels of reactive species, the mortality induced by juglone and ameliorate the deficits in odorant preference associative learning of the worms. However, the chronic treatment with DPDS also induced a decreased of movement and a raise of the paralysis induced by Ab. This results indicate that despite the protective effects in oxidative stress and memory provided by DPDS, it exacerbate the toxic effects of Ab in the body wall muscles of the transgenic worms, suggesting that the toxicity of this peptide not only occurs by oxidative stress. Thereby, more studies are necessary to understand how exactly the Ab peptide induces toxicity in C. elegans model and how the DPDS acts to exerts its protective effects in the worms.