Metals, oxidative stress, and neurodegenerative disorders: Alzheimer's disease (AD) and Parkinson's disease (PD) are age-related disorders characterized by abnormal protein deposits in the brain. AD is marked by amyloid plaques and neurofibrillary tangles, while PD involves the loss of dopaminergic neurons and Lewy bodies. Oxidative stress, caused by reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a key factor in these diseases. Metals like iron (Fe), copper (Cu), and zinc (Zn) play a role in oxidative stress, with Fe and Cu being redox-active and contributing to free radical formation. Increased oxidative stress in AD is associated with higher levels of Fe and Cu, protein and DNA oxidation, lipid peroxidation, and reduced cytochrome c oxidase activity. In PD, oxidative stress is linked to the substantia nigra pars compacta, with markers like 4-hydroxytrans-2-nonenal (HNE) indicating lipid peroxidation. Other factors, including inflammation, nitric oxide toxicity, and mitochondrial dysfunction, also contribute to PD. Antioxidants such as glutathione, vitamin C, vitamin E, lipoic acid, flavonoids, and curcumin may protect against oxidative stress. The article discusses the role of redox metals in the etiology of AD and PD, emphasizing metal-induced free radical formation and antioxidant protection. It also explores the "alternate hypothesis" regarding AD, suggesting that amyloid-β (Aβ) may not be the initiating event but a secondary factor. The biochemistry of metal-induced oxidative stress involves free radicals, particularly superoxide anion radicals, which can generate other ROS through enzymatic or metal-catalyzed reactions. Iron regulation is crucial, as excessive superoxide can release free iron, leading to the Fenton reaction and hydroxyl radical formation. This review highlights the importance of understanding metallo-neurobiology and antioxidant mechanisms in the pathogenesis of neurodegenerative disorders.Metals, oxidative stress, and neurodegenerative disorders: Alzheimer's disease (AD) and Parkinson's disease (PD) are age-related disorders characterized by abnormal protein deposits in the brain. AD is marked by amyloid plaques and neurofibrillary tangles, while PD involves the loss of dopaminergic neurons and Lewy bodies. Oxidative stress, caused by reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a key factor in these diseases. Metals like iron (Fe), copper (Cu), and zinc (Zn) play a role in oxidative stress, with Fe and Cu being redox-active and contributing to free radical formation. Increased oxidative stress in AD is associated with higher levels of Fe and Cu, protein and DNA oxidation, lipid peroxidation, and reduced cytochrome c oxidase activity. In PD, oxidative stress is linked to the substantia nigra pars compacta, with markers like 4-hydroxytrans-2-nonenal (HNE) indicating lipid peroxidation. Other factors, including inflammation, nitric oxide toxicity, and mitochondrial dysfunction, also contribute to PD. Antioxidants such as glutathione, vitamin C, vitamin E, lipoic acid, flavonoids, and curcumin may protect against oxidative stress. The article discusses the role of redox metals in the etiology of AD and PD, emphasizing metal-induced free radical formation and antioxidant protection. It also explores the "alternate hypothesis" regarding AD, suggesting that amyloid-β (Aβ) may not be the initiating event but a secondary factor. The biochemistry of metal-induced oxidative stress involves free radicals, particularly superoxide anion radicals, which can generate other ROS through enzymatic or metal-catalyzed reactions. Iron regulation is crucial, as excessive superoxide can release free iron, leading to the Fenton reaction and hydroxyl radical formation. This review highlights the importance of understanding metallo-neurobiology and antioxidant mechanisms in the pathogenesis of neurodegenerative disorders.