Oxidative stress is a key factor in the pathogenesis of Alzheimer's disease (AD), which is characterized by the accumulation of amyloid-beta (Aβ) peptides and neurofibrillary tangles. Aβ is a 38-43 amino acid peptide derived from the amyloid precursor protein (APP) through cleavage by β- and γ-secretases. Aβ aggregates into β-sheet rich fibrils, forming amyloid plaques in the brain. These plaques are often associated with metal ions such as copper, iron, and zinc, which can catalyze the production of reactive oxygen species (ROS), leading to oxidative damage on Aβ and surrounding molecules. ROS, including hydroxyl radicals, can cause oxidative damage to proteins, lipids, and nucleic acids, contributing to the progression of AD. Metal ions, particularly copper and iron, play a significant role in AD pathogenesis. They can bind to Aβ and modulate its aggregation, which is a key step in the formation of amyloid plaques. The interaction between Aβ and metal ions can lead to the production of ROS, which further exacerbates oxidative damage. Additionally, metal ions can disrupt the function of proteins and enzymes involved in cellular processes, such as ATP production and DNA repair, contributing to neuronal dysfunction and death. Oxidative stress is also linked to the formation of neurofibrillary tangles, which are composed of hyperphosphorylated tau protein. Oxidative damage can alter the structure and function of tau, promoting the formation of neurofibrillary tangles. Furthermore, oxidative stress can impair the clearance of Aβ from the brain, leading to its accumulation and further damage. The role of metal ions in AD is complex, as they can act as both pro-oxidants and antioxidants depending on their coordination environment. The balance of metal ions in the brain is crucial for maintaining cellular homeostasis. Disruptions in metal homeostasis, such as increased levels of copper or iron, can lead to oxidative stress and contribute to the progression of AD. In summary, oxidative stress and metal ion interactions are central to the pathogenesis of AD. The accumulation of Aβ and metal ions, along with the production of ROS, leads to oxidative damage on Aβ and surrounding molecules, contributing to the neurodegenerative processes observed in AD. Understanding these mechanisms is essential for developing therapeutic strategies to combat AD.Oxidative stress is a key factor in the pathogenesis of Alzheimer's disease (AD), which is characterized by the accumulation of amyloid-beta (Aβ) peptides and neurofibrillary tangles. Aβ is a 38-43 amino acid peptide derived from the amyloid precursor protein (APP) through cleavage by β- and γ-secretases. Aβ aggregates into β-sheet rich fibrils, forming amyloid plaques in the brain. These plaques are often associated with metal ions such as copper, iron, and zinc, which can catalyze the production of reactive oxygen species (ROS), leading to oxidative damage on Aβ and surrounding molecules. ROS, including hydroxyl radicals, can cause oxidative damage to proteins, lipids, and nucleic acids, contributing to the progression of AD. Metal ions, particularly copper and iron, play a significant role in AD pathogenesis. They can bind to Aβ and modulate its aggregation, which is a key step in the formation of amyloid plaques. The interaction between Aβ and metal ions can lead to the production of ROS, which further exacerbates oxidative damage. Additionally, metal ions can disrupt the function of proteins and enzymes involved in cellular processes, such as ATP production and DNA repair, contributing to neuronal dysfunction and death. Oxidative stress is also linked to the formation of neurofibrillary tangles, which are composed of hyperphosphorylated tau protein. Oxidative damage can alter the structure and function of tau, promoting the formation of neurofibrillary tangles. Furthermore, oxidative stress can impair the clearance of Aβ from the brain, leading to its accumulation and further damage. The role of metal ions in AD is complex, as they can act as both pro-oxidants and antioxidants depending on their coordination environment. The balance of metal ions in the brain is crucial for maintaining cellular homeostasis. Disruptions in metal homeostasis, such as increased levels of copper or iron, can lead to oxidative stress and contribute to the progression of AD. In summary, oxidative stress and metal ion interactions are central to the pathogenesis of AD. The accumulation of Aβ and metal ions, along with the production of ROS, leads to oxidative damage on Aβ and surrounding molecules, contributing to the neurodegenerative processes observed in AD. Understanding these mechanisms is essential for developing therapeutic strategies to combat AD.