Redox changes and cellular senescence are key factors in the pathogenesis of Alzheimer's disease (AD). Abnormal accumulation of beta-amyloid (Aβ), tau protein, and heme dyshomeostasis lead to increased reactive oxygen species (ROS), which damage cellular components such as proteins, DNA, and lipids, impairing neuronal function and causing cell death. ROS also induce cellular senescence, which exacerbates inflammation and tissue dysfunction. Cellular senescence is characterized by the accumulation of senescent cells, which release pro-inflammatory factors and contribute to neurodegeneration. The interplay between oxidative stress, cellular senescence, and other pathological processes such as mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and heme/iron dyshomeostasis is central to AD progression. Aβ and tau proteins contribute to redox dyshomeostasis by altering mitochondrial function, synaptic dysfunction, and calcium homeostasis. Heme dyshomeostasis also plays a role in AD, as excess heme can promote oxidative stress and neuronal damage. Mitochondrial dysfunction is a major source of ROS, and damaged mitochondria further exacerbate oxidative stress and cellular senescence. ER stress is closely linked to oxidative stress, as protein folding in the ER requires a controlled redox environment. ER stress can enhance γ-secretase activity, leading to increased Aβ production and aggregation. Therapeutic strategies targeting redox imbalances, including antioxidant treatments, heme/iron chelation, and senolytic agents, are being explored for AD. While some interventions show promise, further research is needed to translate these findings into effective clinical treatments.Redox changes and cellular senescence are key factors in the pathogenesis of Alzheimer's disease (AD). Abnormal accumulation of beta-amyloid (Aβ), tau protein, and heme dyshomeostasis lead to increased reactive oxygen species (ROS), which damage cellular components such as proteins, DNA, and lipids, impairing neuronal function and causing cell death. ROS also induce cellular senescence, which exacerbates inflammation and tissue dysfunction. Cellular senescence is characterized by the accumulation of senescent cells, which release pro-inflammatory factors and contribute to neurodegeneration. The interplay between oxidative stress, cellular senescence, and other pathological processes such as mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and heme/iron dyshomeostasis is central to AD progression. Aβ and tau proteins contribute to redox dyshomeostasis by altering mitochondrial function, synaptic dysfunction, and calcium homeostasis. Heme dyshomeostasis also plays a role in AD, as excess heme can promote oxidative stress and neuronal damage. Mitochondrial dysfunction is a major source of ROS, and damaged mitochondria further exacerbate oxidative stress and cellular senescence. ER stress is closely linked to oxidative stress, as protein folding in the ER requires a controlled redox environment. ER stress can enhance γ-secretase activity, leading to increased Aβ production and aggregation. Therapeutic strategies targeting redox imbalances, including antioxidant treatments, heme/iron chelation, and senolytic agents, are being explored for AD. While some interventions show promise, further research is needed to translate these findings into effective clinical treatments.