Bcl-2 Overexpression Protects Against Amyloid-Beta and Prion Toxicity in GT1-7 Neural Cells

In this study we analysed the effect of Bcl-2 on the cytotoxicity induced by the amyloid-β (Aβ_25–35) and prion (PrP_106–126) peptides by using GT1-7 puro and GT1-7 bcl-2 (overexpressing the anti-apoptotic protein Bcl-2) neural cells. Exposure to Aβ_25–35 (1–5 μM) and PrP_106–126 (25 μM) caused a decrease in cell viability, as determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. These data were correlated with Aβ_25–35 and PrP_106–126-induced activation of caspase-9, which is linked to the mitochondrial death pathway, and the activation of the effector caspase-3, suggesting cell death by apoptosis. Furthermore, Bcl-2 overexpression protected from loss of cell viability and caspase-9 and -3 activation induced by Aβ_25–35 and PrP_106–126, showing that Bcl-2 is neuroprotective against apoptotic cell death caused by amyloidogenic peptides.