Exposure to Chlorpyrifos and Mitochondrial Dysfunction in a Striatal Cell Model of Huntington’s Disease

Gifty Dominah, Oberlin College

Location

Science Center, A255

Document Type

Presentation

Start Date

4-24-2015 4:00 PM

End Date

4-24-2015 5:30 PM

Abstract

Despite the genetic cause of Huntington’s disease (HD), emerging evidence suggests that potential exposure to environmental factors may contribute to the variability in the age of onset, progression, and severity of the disorder. Recognizing some of the shared similarities in the pathophysiological mechanisms in HD and pesticide neurotoxicity such as oxidative stress and mitochondrial dysfunction, we hypothesized that the commonly used pesticide chlorpyrifos would exhibit a disease-toxicant interaction and reveal the influence of CPF in HD neuropathology. Our results suggest that expression of mutant HD protein potentiates CPF neurotoxicity via oxidative stress and mitochondrial dysfunction pathways to cause striatal neuron loss.

Notes

Session 3, Panel 18 - Nature vs. Nurture Remixed: Studies in Regulation, Regeneration, Isolation, and Degradation
Moderator: Gunnar Kwakye, Assistant Professor of Neuroscience

Major

Neuroscience

Advisor(s)

Gunnar Kwakye, Neuroscience

Project Mentor(s)

Gunnar Kwakye, Neuroscience

April 2015

This document is currently not available here.

Share

COinS
 
Apr 24th, 4:00 PM Apr 24th, 5:30 PM

Exposure to Chlorpyrifos and Mitochondrial Dysfunction in a Striatal Cell Model of Huntington’s Disease

Science Center, A255

Despite the genetic cause of Huntington’s disease (HD), emerging evidence suggests that potential exposure to environmental factors may contribute to the variability in the age of onset, progression, and severity of the disorder. Recognizing some of the shared similarities in the pathophysiological mechanisms in HD and pesticide neurotoxicity such as oxidative stress and mitochondrial dysfunction, we hypothesized that the commonly used pesticide chlorpyrifos would exhibit a disease-toxicant interaction and reveal the influence of CPF in HD neuropathology. Our results suggest that expression of mutant HD protein potentiates CPF neurotoxicity via oxidative stress and mitochondrial dysfunction pathways to cause striatal neuron loss.