The review discusses the role of redox dysregulation and cellular senescence in Alzheimer's disease (AD). It highlights how elevated reactive oxygen species (ROS) levels, caused by abnormal accumulation of beta-amyloid peptide (Aβ), tau protein, and heme dyshomeostasis, contribute to neuronal dysfunction and cell death. Excessive ROS damages cellular components, leading to impaired neuronal function and cell death. Cellular senescence, triggered by oxidative stress, further exacerbates inflammation and tissue dysfunction. The review also explores the intricate relationship between redox reactions, cellular senescence, Aβ, tau proteins, heme dyshomeostasis, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction in AD. Additionally, it examines therapeutic interventions targeting these pathways, including antioxidant treatments, heme/iron chelators, metal ion chelators, acetylcholinesterase inhibitors, and senolytic agents. While some interventions have shown promise, more research is needed to translate these findings into clinical applications.The review discusses the role of redox dysregulation and cellular senescence in Alzheimer's disease (AD). It highlights how elevated reactive oxygen species (ROS) levels, caused by abnormal accumulation of beta-amyloid peptide (Aβ), tau protein, and heme dyshomeostasis, contribute to neuronal dysfunction and cell death. Excessive ROS damages cellular components, leading to impaired neuronal function and cell death. Cellular senescence, triggered by oxidative stress, further exacerbates inflammation and tissue dysfunction. The review also explores the intricate relationship between redox reactions, cellular senescence, Aβ, tau proteins, heme dyshomeostasis, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction in AD. Additionally, it examines therapeutic interventions targeting these pathways, including antioxidant treatments, heme/iron chelators, metal ion chelators, acetylcholinesterase inhibitors, and senolytic agents. While some interventions have shown promise, more research is needed to translate these findings into clinical applications.