Event Title
A Disease-Toxicant Interaction Reveals Cadmium Exposure as a Potential Modulator in Huntington’s Disease Neuropathology
Location
Science Center, Bent Corridor
Start Date
9-26-2014 12:00 PM
End Date
9-26-2014 1:20 PM
Poster Number
33
Abstract
Huntington’s disease (HD) is a congenital neurological disorder that presents with selective neuronal loss in the striatum of the brain. A genetic mutation in the HTT gene results in overproduction of the amino acid glutamine in the HTT protein, and also results in motor dysfunction and psychiatric and cognitive deficiencies. The HTT protein is ubiquitously expressed in the body with critical functions in neurodevelopment and metal transport, yet more remains to be known about the protein’s role. In spite of the genetic cause of HD, there is emerging evidence that suggests that environmental factors may contribute to the variability in age of onset, disease progression, and symptomology. Interestingly, heavy metal neurotoxicity and HD share similarities in cellular targets, including disregulated metal homeostasis, protein aggregation, and oxidative stress. Thus, our overarching research goal is to understand the basis of the selective neuropathology seen in HD by investigating cadmium neurotoxicity within the common targets of neuropathology to ultimately glean insights about HD neuropathology.
Recommended Citation
Korley, Edmund, "A Disease-Toxicant Interaction Reveals Cadmium Exposure as a Potential Modulator in Huntington’s Disease Neuropathology" (2014). Celebration of Undergraduate Research. 9.
https://digitalcommons.oberlin.edu/cour/2014/posters/9
Award
Oberlin College Research Fellow (OCRF)
Project Mentor(s)
Gunnar Kwakye, Neuroscience
Document Type
Poster
A Disease-Toxicant Interaction Reveals Cadmium Exposure as a Potential Modulator in Huntington’s Disease Neuropathology
Science Center, Bent Corridor
Huntington’s disease (HD) is a congenital neurological disorder that presents with selective neuronal loss in the striatum of the brain. A genetic mutation in the HTT gene results in overproduction of the amino acid glutamine in the HTT protein, and also results in motor dysfunction and psychiatric and cognitive deficiencies. The HTT protein is ubiquitously expressed in the body with critical functions in neurodevelopment and metal transport, yet more remains to be known about the protein’s role. In spite of the genetic cause of HD, there is emerging evidence that suggests that environmental factors may contribute to the variability in age of onset, disease progression, and symptomology. Interestingly, heavy metal neurotoxicity and HD share similarities in cellular targets, including disregulated metal homeostasis, protein aggregation, and oxidative stress. Thus, our overarching research goal is to understand the basis of the selective neuropathology seen in HD by investigating cadmium neurotoxicity within the common targets of neuropathology to ultimately glean insights about HD neuropathology.