Date of Award

2017

Document Type

Dissertation/Thesis

Submission Date

October 2026

Thesis/Dissertation Advisor [Chair]

Wetterer, James K.

Abstract

Aging is the result of the progressive and intrinsic accumulation of detrimental changes in an organism over time. Understanding the molecular pathways that contribute to aging is critical for the development of therapeutic agents to treat age-related disorders. As an animal ages, it accumulates senescent cells, cells that are unable to grow or divide but remain metabolically active. They secrete Senescence Associated Secretory Phenotype (SASP) factors, which can disrupt tissue and cause age related diseases. The Ercc1-/Δ mice are an accelerated aging, progeriod model, and thus it was hypothesized that cellular senescence would increase in the Ercc1-/Δ mice. Through quantitative polymerase chain reaction (qPCR) analysis, the expression of senescence biomarkers p16INK4a, p21, IL-6 and TNF-α were measured to confirm that Ercc1-/Δ mice do experience an increase in cellular senescence. Additionally, we were able to determine that there are gender differences regarding the accumulation of senescent cells in various body parts.

Comments

Includes bibliography.

Extent

38 p.

Identifier

FA00012609

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