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Fig. 3 | Journal of Biomedical Science

Fig. 3

From: Oxidative toxicity in diabetes and Alzheimer’s disease: mechanisms behind ROS/ RNS generation

Fig. 3

Production and mechanism of oxidative stress in AD. Brain consumes more oxygen than the whole body, and is a rich source of fatty acids and metals that are more susceptible to oxidative damage in AD. Two main hallmarks of AD i.e. Aβ plaques and hyper-phosphorylated tau neurofibrillary tangles (T-NFTs) are involved in production as well as promotion of oxidative damage. Any abnormal increase in ROS due to presence of Aβ and NFTs promote mitochondrial DNA/ RNA damage that resulted in mitochondrial dysfunction and membrane damage. Other damages associated with oxidative stress in AD are autoxidation of glucose that resulted in production of AGES and alternatively induce Aβ- toxicity. As oxidative stress, itself induce Aβ and NFTs formation, the result is induced apoptosis, neuronal death and impaired synapsis

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