The Effect of Nicotinamide Supplementation on Lifespan, Reproduction, and Gene Expression of Caenorhabditis Elegans

The leading risk for many diseases such as neurodegenerative, cardiovascular, and Type-2 diabetes, is aging. Nicotinamide adenine dinucleotide (NAD+) is one of the most important coenzymes and cofactors in metabolism, playing a role in numerous pathways and metabolomic functions. However, previous studies have shown a decline in NAD+ with aging, suggesting a connection between NAD+ metabolism and age-related diseases.

Nicotinamide (NAM) is a precursor of NAD+. Specifically, NAM is produced when NAD+ is metabolized by enzymes such as Sirtuins or Poly(ADP-ribosyl) polymerases (PARPs). However, in the salvage pathway, NAD+ is recovered from NAM, which involves nicotinamide mononucleotide (NMN) as an intermediate. Therefore, an increase in NAM and NMN levels could potentially increase NAD+ levels. With my project, I aimed to investigate whether NAM supplementation could boost NAD+ levels and positively counteract age related decline. To do this, I examined supplementation of NAM on reproduction and lifespan in the model organism C. elegans.

Previous studies suggest that NMN, the intermediate between NAM and NAD+ in the salvage pathway, could act as an anti-aging supplement. Knowing this, I hypothesized C. Elegans will have an increase in lifespan with supplementation of NAM. Contradicting previous literature, my work has shown NAM has a dose-dependent decrease in lifespan, with higher doses (10mM-25mM) decreasing lifespan.

A limitation of this study is the lack of biological replicates, therefore decreasing the significance of the observed results. To confirm the results found, these experiments should be repeated a minimum of two more times. In addition to repeating the performed assays, more experiments such as protein expression using Western Blots could provide deeper insight into the reason behind the decline of lifespan.

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Work Title The Effect of Nicotinamide Supplementation on Lifespan, Reproduction, and Gene Expression of Caenorhabditis Elegans
Subtitle Science Research Distinction (SCIRES)
Access
Open Access
Creators
  1. Andrew Spence
Keyword
  1. SCIRES
  2. Caenorhabditis Elegans
  3. Metabolism
  4. Nicotinamide
License In Copyright (Rights Reserved)
Work Type Research Paper
Acknowledgments
  1. Dr. Melanie McReynolds
  2. Abdulkareem Alshaheeb
Publication Date May 9, 2025
Deposited May 09, 2025

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Version 1
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  • Created

    May 09, 2025 09:55 by ams10637

  • Updated

    May 09, 2025 09:55 by [unknown user]

  • Updated Keyword, Subtitle, Description, and 1 more Show Changes

    May 09, 2025 09:58 by ams10637

    Keyword
    • SCIRES, Caenorhabditis Elegans, Metabolism, Nicotinamide
    Subtitle
    • Science Research Distinction (SCIRES)
    Description
    • The leading risk for many diseases such as neurodegenerative, cardiovascular, and Type-2 diabetes, is aging1. Nicotinamide adenine dinucleotide (NAD+) is one of the most important coenzymes and cofactors in metabolism, playing a role in numerous pathways and metabolomic functions. However, previous studies have shown a decline in NAD+ with aging2, suggesting a connection between NAD+ metabolism and age-related diseases.
    • Nicotinamide (NAM) is a precursor of NAD+. Specifically, NAM is produced when NAD+ is metabolized by enzymes such as Sirtuins or Poly(ADP-ribosyl) polymerases (PARPs). However, in the salvage pathway, NAD+ is recovered from NAM, which involves nicotinamide mononucleotide (NMN) as an intermediate. Therefore, an increase in NAM and NMN levels could potentially increase NAD+ levels. With my project, I aimed to investigate whether NAM supplementation could boost NAD+ levels and positively counteract age related decline. To do this, I examined supplementation of NAM on reproduction and lifespan in the model organism C. elegans.
    • Previous studies suggest that NMN, the intermediate between NAM and NAD+ in the salvage pathway, could act as an anti-aging supplement3. Knowing this, I hypothesize C. Elegans will have an increase in lifespan with supplementation of NAM. Contradicting previous literature, my work has shown NAM has a dose-dependent decrease in lifespan, with higher doses (10mM-25mM) decreasing lifespan.
    • A limitation of this study is the lack of biological replicates, therefore decreasing the significance of the observed results. To confirm the results found, these experiments should be repeated a minimum of two more times. In addition to repeating the performed assays, more experiments such as protein expression using Western Blots could provide deeper insight into the reason behind the decline of lifespan.
    Publication Date
    • 2025-05-09
  • Updated Acknowledgments Show Changes

    May 09, 2025 09:59 by ams10637

    Acknowledgments
    • Dr. Melanie McReynolds, Abdulkareem Alshaheeb
  • Added Creator Andrew Spence

    May 09, 2025 09:59 by ams10637

  • Added SpenceAndrew SCIRES Thesis Final.docx

    May 09, 2025 09:59 by ams10637

  • Updated Description, License Show Changes

    May 09, 2025 10:10 by ams10637

    Description
    • The leading risk for many diseases such as neurodegenerative, cardiovascular, and Type-2 diabetes, is aging1. Nicotinamide adenine dinucleotide (NAD+) is one of the most important coenzymes and cofactors in metabolism, playing a role in numerous pathways and metabolomic functions. However, previous studies have shown a decline in NAD+ with aging2, suggesting a connection between NAD+ metabolism and age-related diseases.
    • The leading risk for many diseases such as neurodegenerative, cardiovascular, and Type-2 diabetes, is aging. Nicotinamide adenine dinucleotide (NAD+) is one of the most important coenzymes and cofactors in metabolism, playing a role in numerous pathways and metabolomic functions. However, previous studies have shown a decline in NAD+ with aging, suggesting a connection between NAD+ metabolism and age-related diseases.
    • Nicotinamide (NAM) is a precursor of NAD+. Specifically, NAM is produced when NAD+ is metabolized by enzymes such as Sirtuins or Poly(ADP-ribosyl) polymerases (PARPs). However, in the salvage pathway, NAD+ is recovered from NAM, which involves nicotinamide mononucleotide (NMN) as an intermediate. Therefore, an increase in NAM and NMN levels could potentially increase NAD+ levels. With my project, I aimed to investigate whether NAM supplementation could boost NAD+ levels and positively counteract age related decline. To do this, I examined supplementation of NAM on reproduction and lifespan in the model organism C. elegans.
    • Previous studies suggest that NMN, the intermediate between NAM and NAD+ in the salvage pathway, could act as an anti-aging supplement3. Knowing this, I hypothesize C. Elegans will have an increase in lifespan with supplementation of NAM. Contradicting previous literature, my work has shown NAM has a dose-dependent decrease in lifespan, with higher doses (10mM-25mM) decreasing lifespan.
    • Previous studies suggest that NMN, the intermediate between NAM and NAD+ in the salvage pathway, could act as an anti-aging supplement. Knowing this, I hypothesized C. Elegans will have an increase in lifespan with supplementation of NAM. Contradicting previous literature, my work has shown NAM has a dose-dependent decrease in lifespan, with higher doses (10mM-25mM) decreasing lifespan.
    • A limitation of this study is the lack of biological replicates, therefore decreasing the significance of the observed results. To confirm the results found, these experiments should be repeated a minimum of two more times. In addition to repeating the performed assays, more experiments such as protein expression using Western Blots could provide deeper insight into the reason behind the decline of lifespan.
    License
    • https://rightsstatements.org/page/InC/1.0/
  • Published

    May 09, 2025 10:10 by ams10637

  • Updated

    May 09, 2025 22:05 by [unknown user]