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| Abstract |
Neurodegenerative diseases are becoming more common in today’s world. Two of the more prominent diseases that fall into this category are multiple sclerosis (MS) and Alzheimer’s disease (AD). A hallmark for both of these diseases is mitochondrial dysfunction. Mitochondrial dysfunction causes an increase in the number of damaged mitochondria, which is linked to a decrease in the energy supply for the cell. Mitophagy is a mechanism known for eliminating damaged mitochondria and is impaired in neurodegenerative diseases. This causes an accumulation of damaged mitochondria in the cell leading to loss of function. We have also shown that a dietary factor known as betaine, is able to restore energy production within the dysfunctional mitochondria. In the present study, we are investigating the role of betaine in both AD and cuprizone mouse models, hypothesizing that betaine will restore energy production by eliminating damaged mitochondria using mitophagy.
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| Contributor(s) |
Faculty Mentor
Jennifer McDonough Ernest Freeman
Sarah Sternbach
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| Modified Abstract |
Neurodegenerative diseases are becoming more common in today’s world. Two of the more prominent diseases that fall into this category are multiple sclerosis (MS) and Alzheimer’s disease (AD). A hallmark for both of these diseases is mitochondrial dysfunction. Mitochondrial dysfunction causes an increase in the number of damaged mitochondria, which is linked to a decrease in the energy supply for the cell. Mitophagy is a mechanism known for eliminating damaged mitochondria and is impaired in neurodegenerative diseases. In the present study, we are investigating the role of betaine in both AD and cuprizone mouse models, hypothesizing that betaine will restore energy production by eliminating damaged mitochondria using mitophagy. |