Huntington disease (HD) is a neurodegenerative disorder caused by expansion of a polyglutamine tract within the huntingtin (HTT) protein, forming mutant HTT (mtHTT). HD patients suffer from psychiatric, behavioral, cognitive, and motor abnormalities, with death typically occurring 15-20 years after symptom onset. Currently, there are no treatments able to slow disease progression or delay onset. HD is a disease of aging. Despite the mtHTT protein being produced throughout life, symptoms do not typically appear until adulthood. Furthermore, many cellular effects of normal aging are also seen in HD, including altered intercellular communication and loss of proteostasis. Recently, our lab found evidence that inducing age-like changes uncovers HD phenotypes, which contribute to pathogenesis in neurons. This suggests that reversing the aging process could counteract phenotypic development of HD. Thus, anti-aging could be effective for treatment of HD. Our lab conducted an anti-aging preclinical trial in which aged HD mice were systematically treated with plasma from young mice, known as young blood treatment. The goal of this trial was to investigate if treatment could successfully delay disease onset or progression. The aim of my project is to determine if treatment affected biological age and HD by analyzing the levels of protein markers in these brains. Preliminary data validates that aging markers decrease with age and shows that young blood treatment has varying success at rejuvenating protein levels. This work contributes to a better understanding of the relationship between biological age and HD pathogenesis.

Thesis Completion




Thesis Chair/Advisor

Southwell, Amber L.


Bachelor of Science (B.S.)


College of Medicine


Burnett School of Biomedical Sciences

Degree Program

Biomedical Sciences



Access Status

Open Access

Release Date