“…Aβs have been reported to induce apoptosis in neuronal cells by mitochondrial dysfunction and oxidative 2 , and incubated to achieve complete cell attachment. Cells were treated for 4,8,12,48,72 stress (10), alteration of metal ion influx (11), endoplasmic reticulum stress (12) and impaired autophagy (13). In order to test the generality of cell protective activity of SE, we investigated here whether SE protects the neuronal cell death induced by amyloid β-peptides (Aβ and Aβ [25][26][27][28][29][30][31][32][33][34][35] ).…”