Elham Rezvani Boroujeni - Department of Microbiology and Microbial Biotechnology, Faculty of Life Science and Biotechnology, Shahid Beheshti University, Tehran, Iran and Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale G.B Morgagni ۵۰, ۵۰۱
Seyed Masoud Hosseini - Department of Microbiology and Microbial Biotechnology, Faculty of Life Science and Biotechnology, Shahid Beheshti University, Tehran, Iran
Cristina Cecchi - Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale G.B Morgagni ۵۰, ۵۰۱۳۴ Florence, Italy
Fabrizio Chiti - Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale G.B Morgagni ۵۰, ۵۰۱۳۴ Florence, Italy

Background and Aim : Alzheimer's disease (AD) is the most prevalent form of dementia caused by accumulation of senile plaques formed by AB. Cellular prion protein (PrPC) is a membrane protein and that has a high binding affinity for Aβ۴۲ oligomers. The levels of reactive oxygen species (ROS) and Ca۲+ were investigated in human neuroblastoma cells after treatment with Aβ۴۲ oligomers (ADDLs) in presence and absence of short prion-derived peptide.Methods : SH-SY۵Y neuroblastoma cells were seeded on glass coverslip in ۶ well plates. After ۲۴ h, ۶۰۰ μl of various samples were added to cells and after washing, cells loaded with Fluo-۴ AM and CM-H۲DFDA specific probe for Ca۲+ and ROS, respectively. Cell image acquisition was performed using the TCS SP۸ confocal system and analysis was done using Image J software.Results : The quantification of the intracellular Ca۲+ and ROS derived fluorescence shows that the treatment of the cells with A?۴۲ ADDLs causes an increase of intracellular Ca۲+ and ROS compared with untreated cells and when cells were treated with A?۴۲ ADDLs + synthetic peptides ROS and Ca۲+ levels were significantly lower than those observed after treatment with A?۴۲ ADDLs alone.Conclusion : The present study shows the synthetic peptide can effectively protect the SH-SY۵Y cells against the oxidative stress and Ca۲+ influx induced by Aβ۴۲ ADDLs and has potential therapeutic value for the treatment of AD.

Prion protein, AB oligomer, Alzheimer's disease, ADDLs