There is strong evidence thatb-amyloid (Ab) causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer’s dis-ease. Mitochondrial transcription factor A (Tfam) has multiple roles in the maintenance of mtDNA. To study the protective roles of Tfam against amyloid neurotoxicity, we established SH-SY5Y cell lines stably over-expressing Tfam and exposed them to 10lmAb1-42 for 24 h.