Novel Compound Screening to Combat Huntingtin Protein Aggregation in a Transgenic C. elegans Model.

Riley Kane*, Jacob Boos, Werner Geldenhuys, Ph.D.
Health Sciences Center, West Virginia University, Morgantown, WV, 26505

Presentation Category: Health Sciences (Poster presentation)

Student’s Major: Biochemistry

Huntington’s Disease (HD) is a progressive, neurodegenerative disorder currently affecting nearly 30,000 people in the United States, while another 200,000 are genetically predisposed to disease development. The average age of onset is around 30-50 years of age, with patients presenting clinical symptoms that include cognitive impairment, uncontrollable movements (chorea), behavioral disturbances, and dementia. Hallmark pathology of HD includes aggregation of the huntingtin protein (Htt) due to increased polyglutamine repeats. In HD, Htt proteins aggregate within the striatum, substantia nigra, varying layers of the cerebral cortex, hippocampus, cerebellum, and parts of the hypothalamus and thalamus. Htt aggregation increases brain oxidative stress, thus killing neurons and progressing the disease. While there is no cure for HD, this study aims to screen novel compounds using a transgenic Caenorhabditis elegans model of HD that expresses various lengths of the Htt protein, examining the effects of our compounds on lifespan, Htt aggregation, and neuronal death.

Funding: NIH

Program/mechanism supporting research/creative efforts: WVU's Research Apprenticeship Program (RAP) & accompanying HONR 297-level course, NIH