Efeito dos compostos orgânicos de selênio - ebselen e disseleneto de difenila - na morte neuronal causada pelo peptídeo beta-amilóide em culturas primárias de neurônio de hipocampo de rato

Abstract

Alzheimer s disease (AD) is the most common form of dementia among elder. Neuropathological hallmarks include amyloid plaque formation, neurofibrillary tangles, neuronal and synaptic loss. The deposit of senile plaques is consistent with induction of oxidative stress, and since free radical scavengers can alleviate amyloid-beta-induced oxidative stress markers, this study aims to identify the neuroprotective effects of the selenium compounds (ebselen and diphenyl diselenide) on the neurotoxicity of amyloid-beta in primary cultures of murine hippocampal neurons. Samples were subjected to immunocytochemistry and western blotting techniques to determine what influence the treatments may have on synaptic protein SNAP-25 and neuronal death. There was a strong increase in relative cell viability associated with ebselen and diphenyl diselenide treatment. Significant increases were observed in the level of synaptic marker synaptosomal-associated protein SNAP-25 with both selenium compounds treatment. Although demonstrated the potential protective effect of selenium compounds in the course of AD, further investigations of synaptic function are important as a therapeutic strategy for AD