Event Title

A Disease-Toxicant Interaction Reveals Cadmium Exposure as a Potential Modulator in Huntington’s Disease Neuropathology

Presenter Information

Edmund Korley, Oberlin College

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.

Award

Oberlin College Research Fellow (OCRF)

Project Mentor(s)

Gunnar Kwakye, Neuroscience

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Sep 26th, 12:00 PM Sep 26th, 1:20 PM

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.