University of Kentucky

Poster Title

Insight into the Potential Anti-Parkinsonian Effects of a Synthetic, Amidated Eleven Amino Acid Peptide

Institution

University of Kentucky

Abstract

Parkinson’s disease (PD) is a chronic neurodegenerative disease that knows no economic and social boundaries across Kentucky and the nation, affecting over one million Americans each year and expected to double over the next 25 years. While the cause of this disabling disease is unknown, its symptoms manifest following a loss of the neurotransmitter dopamine. While current treatments are able to relieve the physiological symptoms by restoring dopamine levels in the brain, over time they lose their effectiveness as the dopamine-producing neurons continue to be lost as the disease progresses. Thus as a strategy for the long-term treatment of PD, newer approaches should not only restore dopamine levels, but also provide protection to dopamineproducing neurons from further degeneration. Recently, a synthetic, amidated 11-amino acid peptide, was shown to restore dopamine levels in parkinsonian animal models, while providing neuroprotection. Based on our preliminary data, we hypothesized that its molecular and cellular effects involve the mitochondria and the glycolytic protein glyceraldehyde-3-phosphate dehydrogenase, a known drug target for the treatment of PD. We used in vitro enzyme kinetics and cellular protection assays to investigate this potential mechanism of action. Results from this investigation will drive further studies to evaluate the peptide for the treatment of PD.

This document is currently not available here.

Share

COinS
 

Insight into the Potential Anti-Parkinsonian Effects of a Synthetic, Amidated Eleven Amino Acid Peptide

Parkinson’s disease (PD) is a chronic neurodegenerative disease that knows no economic and social boundaries across Kentucky and the nation, affecting over one million Americans each year and expected to double over the next 25 years. While the cause of this disabling disease is unknown, its symptoms manifest following a loss of the neurotransmitter dopamine. While current treatments are able to relieve the physiological symptoms by restoring dopamine levels in the brain, over time they lose their effectiveness as the dopamine-producing neurons continue to be lost as the disease progresses. Thus as a strategy for the long-term treatment of PD, newer approaches should not only restore dopamine levels, but also provide protection to dopamineproducing neurons from further degeneration. Recently, a synthetic, amidated 11-amino acid peptide, was shown to restore dopamine levels in parkinsonian animal models, while providing neuroprotection. Based on our preliminary data, we hypothesized that its molecular and cellular effects involve the mitochondria and the glycolytic protein glyceraldehyde-3-phosphate dehydrogenase, a known drug target for the treatment of PD. We used in vitro enzyme kinetics and cellular protection assays to investigate this potential mechanism of action. Results from this investigation will drive further studies to evaluate the peptide for the treatment of PD.