Oxidative Stress and Mitochondrial Dysfunction in Alzheimer’s Disease

By Xinglong Wang, Wenzhang Wang, Li Li, George Perry, Hyoung-Gon Lee, Xiongwei Zhu. Biochimica et Biophysica Acta, 2013

1,225 citations recorded by the source corpus.

Alzheimer’s disease (AD) exhibits extensive oxidative stress throughout the body, being detected peripherally as well as associated with the vulnerable regions of the brain affected in disease. Abundant evidence not only demonstrates the full spectrum of oxidative damage to neuronal macromolecules, but also reveals the occurrence of oxidative events early in the course of the disease and prior to the formation of the pathology, which support an important role of oxidative stress in AD. As a disease of abnormal aging, AD demonstrats oxidative damage at levels that significantly surpass that of elderly controls, which suggests the involvement of additional factor(s). Structurally and functionally damaged mitochondria, which are more proficient at producing reactive oxygen species but less so in ATP, are also an early and prominent feature of the disease. Since mitochondria are also vulnerable to oxidative stress, it is likely that a vicious downward spiral involving the interactions between mitochondrial dysfunction and oxidative stress contributes to the initiation and/or amplification of reactive oxygen species that is critical to the pathogenesis of AD.

Subfields: Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/a1566b7b308996e53e34c573547a9ab8daf568e9

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In Biochemistry

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2. Geon Ha Kim
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Citations in the corpus

• NOX4 promotes ferroptosis of astrocytes by oxidative stress-induced lipid peroxidation via the impairment of mitochondrial metabolism in Alzheimer's diseases (2021, background): “Oxidative stress from mitochondrial dysfunction occurs in the early stage of AD [7, 8].”
• Ablation of ferroptosis regulator glutathione peroxidase 4 in forebrain neurons promotes cognitive impairment and neurodegeneration (2017, background): “However, concomitant pathological features in AD brains such as augmented inflammation and the chronic nature of the degenerating process cannot be explained by apoptotic cell death alone [3,4].”
• Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “Oxidative stress manifests early in AD, which supports the notion that oxidative stress may drive Aβ-induced AD pathogenesis [99].”
• The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “Second, the activities of key enzymes of oxidative metabolism including α-ketoglutarate dehydrogenase complex, pyruvate dehydrogenase complex, and cytochrome oxidase were reduced in patients with AD [71].”
• Oxidative stress and the amyloid beta peptide in Alzheimer’s disease (2017, background): “Oxidative stress occurs early in the course of AD, which would support its role in AD pathogenesis [48], in relation with the presence of Aβ.”