["Docosahexaenoic acid (DHA, C22:6, n-3) ameliorates the memory-related learning deficits of Alzheimer's disease (AD), which is characterized by fibrillar amyloid deposits in the affected brains. Here, we have investigated whether DHA-induced inhibition of Amyloid β-peptide(25-35) (Aβ(25-35)) fibrillation limits or deteriorates the toxicity of the human neuroblastoma cells (SH-SY5Y).", 'In vitro fibrillation of Aβ(25-35) was performed in the absence or presence of DHA. Afterwards, SH-SY5Y cells were incubated with Aβ(25-35) in absence or presence 20 μM DHA to evaluate its effect on the Aβ(25-35)-induced neurotoxicity by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)]-redox and TUNEL (TdT-mediated dUTP-biotin nick end-labeling) assay and immunohistochemistry. The level of Aβ(25-35)-induced lipid peroxide (LPO) was determined in the absence or presence of oligomer-specific antibody. Fatty acid profile was estimated by gas chromatography.', 'DHA significantly reduced the Aβ(25-35) in vitro fibrillation, as indicated by fluorospectroscopy and transmission electron microscopy. Aβ(25-35) decreased the MTT-redox activity and increased the apoptotic damage and levels of LPO when compared with those of the controls. However, when the SH-SY5Y cells were treated with Aβ(25-35) in the presence of DHA, MTT redox potential significantly increased and the levels LPO decreased, suggesting an inhibition of the Aβ(25-35)-induced neurotoxicity. DHA improved the Aβ(25-35) induced DNA damage and axodendritic loss, with a concomitant increase in the cellular level of DHA, suggesting DHA protects the cell from neurotoxic degeneration.'] Does docosahexaenoic acid withstand the Aβ ( 25-35 ) -induced neurotoxicity in SH-SY5Y cells?