Abstract Title

Peptide Hormone Amylin Reduces Oxidative Stress through Improved Mitochondrial Dynamics

Abstract

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.

Modified Abstract

Oxidative stress has been shown to be a 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 mouse and neuronal cell models of AD (APP/PS1 and Neuroscreen-1 cultures). Although it is apparent that amylin has antioxidant activity, its mechanism of action remains unclear. Because mitochondria are the main contributors to oxidative stress in a cell, they have been a target of our investigation. We have found 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.

Research Category

Biomedical Sciences

Primary Author's Major

Chemistry

Mentor #1 Information

Dr. Gemma Casadesus

Presentation Format

Poster

Start Date

21-3-2017 1:00 PM

Research Area

Molecular and Cellular Neuroscience

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Mar 21st, 1:00 PM

Peptide Hormone Amylin Reduces Oxidative Stress through Improved Mitochondrial Dynamics

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.