Alzheimer's disease (AD) is the most common multifactorial mental illness affecting the elderly population in the world. Its prevalence increases as person ages. There is no known drug or agent that can delay or prevent the AD and its progression. Extensive research has revealed that multiple cellular pathways involved, including amyloid beta production, mitochondrial structural and functional changes, hyperphosphorylation of Tau and NFT formation, inflammatory responses, and neuronal loss in AD pathogenesis. Amyloid beta-induced synaptic damage, mitochondrial abnormalities, and phosphorylated Tau are major areas of present research investigations. Synaptic pathology and mitochondrial oxidative damage are early events in disease process. In this chapter, a systematic literature survey has been conducted and presented a summary of antioxidants used in (1) AD mouse models, (2) elderly populations, and (3) randomized clinical trials in AD patients. This chapter highlights the recent progress in developing and testing mitochondria-targeted molecules using AD cell cultures and AD mouse models. This chapter also discusses recent research on AD pathogenesis and therapeutics, focusing on mitochondria-targeted molecules as potential therapeutic targets to delay or prevent AD progression.