Huntington disease (HD) is a fatal neurodegenerative disease caused by CAG tract expansion in the huntingtin (HTT) gene, which results in production of mutant huntingtin (mtHTT) protein. Although mtHTT is expressed throughout life, onset of HD symptoms typically begins in mid-life, around 35 to 50 years of age. Characteristic HD symptoms include motor, cognitive, and psychiatric abnormalities. The emergence of symptoms in adulthood suggests that aging may play a role in HD pathogenesis. Furthermore, markers of accelerated aging can be observed in HD patients, including telomere attrition, epigenetic alterations, and mitochondrial dysfunction. Our lab has previously observed that induction of age-like changes by treatment with progerin, the mutant protein that causes Hutchinson-Gilford Progeria Syndrome, enhances HD phenotypes and contributes to pathogenesis in HD neurons. Taken together, these findings suggest a link between aging and HD, with implications for potential therapeutic benefits from anti-aging treatment. Our lab has conducted a young blood anti-aging trial in which aged HD and wild-type (WT) mice were injected with plasma from young WT or HD mice. Previous work in our lab confirmed that cortical aging markers decline with age at the protein level and are differentially affected by young blood treatment. In this study, we observed a significant effect of age on striatal expression of aging markers, Grin1 and Lmnb1. Varying effects of young blood anti-aging treatment were observed on the genes of interest.

Thesis Completion




Thesis Chair/Advisor

Southwell, Amber


Bachelor of Science (B.S.)


College of Medicine


Burnett School of Biomedical Sciences

Degree Program

Biomedical Sciences



Access Status

Open Access

Release Date