The article "Oxidative Stress in Alzheimer’s Disease: Current Knowledge of Signaling Pathways and Therapeutics" by Rishika Dhapola et al. explores the role of oxidative stress in the pathophysiology of Alzheimer's disease (AD). The authors highlight that oxidative stress, primarily driven by reactive oxygen species (ROS) generated from mitochondrial dysfunction and other sources, plays a significant role in the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles, leading to neuronal death and cognitive decline. Oxidative stress also triggers apoptosis through the modulation of signaling pathways such as ERK1/2 and Nrf2, resulting in increased GSK-3β expression and decreased PP2A activity. The study reviews the impact of oxidative stress on various signaling pathways, including RCAN1, CREB/ERK, Nrf2, PP2A, NFκB, and PI3K/Akt. It discusses the role of TNF-α in oxidative stress and the potential of drugs like etanercept, pramipexole, memantine, carvedilol, and melatonin in modulating these pathways. Additionally, the article examines the effects of epigallocatechin gallate, genistein, donepezil, and resveratrol on reducing oxidative stress and promoting neuronal survival. The study emphasizes the importance of targeting these pathways for therapeutic advancements in AD.The article "Oxidative Stress in Alzheimer’s Disease: Current Knowledge of Signaling Pathways and Therapeutics" by Rishika Dhapola et al. explores the role of oxidative stress in the pathophysiology of Alzheimer's disease (AD). The authors highlight that oxidative stress, primarily driven by reactive oxygen species (ROS) generated from mitochondrial dysfunction and other sources, plays a significant role in the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles, leading to neuronal death and cognitive decline. Oxidative stress also triggers apoptosis through the modulation of signaling pathways such as ERK1/2 and Nrf2, resulting in increased GSK-3β expression and decreased PP2A activity. The study reviews the impact of oxidative stress on various signaling pathways, including RCAN1, CREB/ERK, Nrf2, PP2A, NFκB, and PI3K/Akt. It discusses the role of TNF-α in oxidative stress and the potential of drugs like etanercept, pramipexole, memantine, carvedilol, and melatonin in modulating these pathways. Additionally, the article examines the effects of epigallocatechin gallate, genistein, donepezil, and resveratrol on reducing oxidative stress and promoting neuronal survival. The study emphasizes the importance of targeting these pathways for therapeutic advancements in AD.