Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, synaptic dysfunction, and neuronal loss. While amyloid-beta plaques and tau neurofibrillary tangles are classical pathological hallmarks, increasing evidence demonstrates that oxidative stress, mitochondrial dysfunction, and neuroinflammation are central drivers of disease progression. Oxidative imbalance leads to lipid peroxidation, protein oxidation, and DNA damage, contributing to neuronal vulnerability. Mitochondrial dysfunction impairs energy metabolism and enhances reactive oxygen species production, further aggravating cellular injury. Concurrently, chronic microglial activation sustains inflammatory responses and amplifies oxidative damage. These interrelated processes create a self-propagating cycle that accelerates neurodegeneration. Understanding their molecular interactions provides new opportunities for therapeutic intervention. This review synthesizes current findings on oxidative stress, mitochondrial abnormalities, and neuroinflammatory mechanisms in AD and highlights emerging treatment strategies targeting these interconnected pathways.