Understanding Mortality and Aging from a Theoretical Model of Damage
Department
Physics
Major
Physics
Research Advisor
Hou, Chen
Advisor's Department
Biological Sciences
Funding Source
Opportunities for Undergraduate Research Experiences (OURE)
Abstract
Modern understanding of oxidative stress at the molecular level has led to a theory of aging which implicates the accumulation of oxidative damage. Dr. Hou previously published a simple theoretical model for the accumulated damage throughout growth and its relationship to longevity, expanding the explanatory power of this theory by demonstrating reduced biosynthesis energy demands result in an increase in energy available for oxidative repair. We successfully simulated mammalian populations from empirical data under an OURE project to verify essential behaviors of the model. Additionally, the population parameters which largely determine the shape of the mortality curve call into question widespread interpretation of certain mortality statistics as aging rate analogues, while allowing us to make simplifying assumptions. We hope to continue improving the model and its application to a wide variety of species. We will address lifespan extension under diet restriction, analyze novel empirical data, and propose better aging statistics.
Biography
Kent Gorday is lab manager of Missouri S&T International Genetically Engineered Machine (iGEM) team and hosts visitors’ nights at the campus observatory. He enjoys playing horn in the Symphony Orchestra and Wind Symphony, photography, and hiking. Kent hopes to pursue graduate education in biophysics after graduating May 2018.
Presentation Type
OURE Fellows Proposal Oral Applicant
Document Type
Presentation
Location
Turner Room
Presentation Date
11 Apr 2017, 10:00 am - 10:20 am
Understanding Mortality and Aging from a Theoretical Model of Damage
Turner Room
Modern understanding of oxidative stress at the molecular level has led to a theory of aging which implicates the accumulation of oxidative damage. Dr. Hou previously published a simple theoretical model for the accumulated damage throughout growth and its relationship to longevity, expanding the explanatory power of this theory by demonstrating reduced biosynthesis energy demands result in an increase in energy available for oxidative repair. We successfully simulated mammalian populations from empirical data under an OURE project to verify essential behaviors of the model. Additionally, the population parameters which largely determine the shape of the mortality curve call into question widespread interpretation of certain mortality statistics as aging rate analogues, while allowing us to make simplifying assumptions. We hope to continue improving the model and its application to a wide variety of species. We will address lifespan extension under diet restriction, analyze novel empirical data, and propose better aging statistics.
