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In Alzheimers disease (AD), both amyloid-beta (A) and hyperphosphorylated microtubule-associated protein tau (MAPT/TAU), the two main pathological hallmarks of AD, accumulate in mitochondria resulting in functional impairment and ROS generation [96,97]

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However, if this response is dysfunctional as a consequence of excessive fibroblast activation and transdifferentiation into myofibroblasts, the cornea can undergo opacification due to excessive irreversible scarification [2]