Oxidative stress has been shown to be an early predictor and key pathological feature of neurodegenerative diseases including Alzheimer’s disease (AD). Previous work in our laboratory has demonstrated that administration of the peptide hormone amylin can reduce levels of oxidative stress in a transgenic mouse model of AD (APP/PS1) as well as Neuroscreen-1 cultures (neuronal cell model). Although it is apparent that amylin has antioxidant activity, its mechanism of action remains unclear. Because mitochondria are the main producers of reactive oxygen species (ROS) that account for oxidative stress in a cell, they have been a target of our investigation. Specifically, we determined whether amylin treatment regulates mitochondrial dynamics-associated proteins and mobility deficits in the APP/PS1 AD mouse model. Our data show that amylin treatment regulates mitochondrial dynamics-associated proteins as well as proteins associated with mitochondrial biogenesis. Taken together, our data suggest that some of the effects of amylin on oxidative stress regulation may stem from improving mitochondrial function.
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