Date of Award

2018

Document Type

Dissertation/Thesis

Submission Date

October 2026

Thesis/Dissertation Advisor [Chair]

Niedernhofer, Laura

Abstract

Aging is the number one risk factor for numerous chronic diseases driving increased morbidity and healthcare costs globally. Thus, finding ways to uncouple chronical aging with risk of disease is imperative. Extensive evidence links aging with increased oxidative stress. The free radical theory of aging posits that reactive oxygen species (ROS) increase with age and cause oxidative damage to cellular components, thereby driving aging. In support of this, overexpressing the endogenous antioxidant catalase specifically in mitochondria (mCAT transgene) improves health and lifespan of mice. I hypothesized that if ROS is a root cause of aging then the mCAT transgene would slow aging in a murine model of a human progeroid syndrome (Ercc1-/Δ mice). Unfortunately, mCAT expression was not highly expressed in all tissues. Nevertheless, mCAT+/-;Ercc1-/Δ mice showed improvements in functional tests and health evaluations relative to Ercc1-/Δ mice supporting the conclusion that ROS plays an important causal role in aging. matching, pre-transplant assessments and allocation of organs. In addition, I will discuss ethical principles that can be used to aid transplant teams in the difficult task of allocating of organs. I will also evaluate alternative options to the current transplant process such as an opt-out vs. an opt-in system and controlled financial payment for organs. Finally, I will analyze current policies regarding living donors and suggest avenues for future research into alternative resources for organs.

Comments

Includes bibliography.

Extent

33 p.

Identifier

FAUHT00016

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