Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by the progressive loss of synapses and cognitive function. Oxidative stress, which involves increased production of reactive oxygen species (ROS) and altered metal homeostasis, plays a significant role in the progression of AD. ROS directly affect synaptic activity and neurotransmission, leading to cognitive dysfunction. The accumulation of amyloid-β (Aβ) and hyperphosphorylated Tau protein, which are hallmarks of AD, further exacerbate mitochondrial dysfunction and ROS production, creating a vicious cycle. While antioxidant therapies have shown mixed results in clinical trials, recent studies suggest that targeting specific mitochondrial functions and ROS production may be more effective. Additionally, non-pharmacological interventions such as exercise and caloric restriction have been shown to have beneficial effects on AD progression by improving mitochondrial function and reducing oxidative stress. Understanding the complex interplay between ROS, mitochondrial dysfunction, and AD pathogenesis is crucial for developing more effective therapeutic strategies.Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by the progressive loss of synapses and cognitive function. Oxidative stress, which involves increased production of reactive oxygen species (ROS) and altered metal homeostasis, plays a significant role in the progression of AD. ROS directly affect synaptic activity and neurotransmission, leading to cognitive dysfunction. The accumulation of amyloid-β (Aβ) and hyperphosphorylated Tau protein, which are hallmarks of AD, further exacerbate mitochondrial dysfunction and ROS production, creating a vicious cycle. While antioxidant therapies have shown mixed results in clinical trials, recent studies suggest that targeting specific mitochondrial functions and ROS production may be more effective. Additionally, non-pharmacological interventions such as exercise and caloric restriction have been shown to have beneficial effects on AD progression by improving mitochondrial function and reducing oxidative stress. Understanding the complex interplay between ROS, mitochondrial dysfunction, and AD pathogenesis is crucial for developing more effective therapeutic strategies.