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Related Concept Videos

Mitochondria01:37

Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
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Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The Effect of Aging on Tissues01:19

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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Related Experiment Video

Updated: Mar 1, 2026

A Suppressor Screen for the Characterization of Genetic Links Regulating Chronological Lifespan in Saccharomyces cerevisiae
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The NAD+/PARP1/SIRT1 Axis in Aging.

Andrew R Mendelsohn1, James W Larrick1

  • 1Panorama Research Institute and Regenerative Sciences Institute , Sunnyvale, California.

Rejuvenation Research
|May 25, 2017
PubMed
Summary

NAD+ levels decrease with age, impairing DNA repair and mitochondrial function. Supplementing with nicotinamide mononucleotide (NMN) restores these functions, suggesting a key role for NAD+ in aging.

Area of Science:

  • Aging research
  • Molecular biology
  • Genetics

Background:

  • NAD+ levels decline with age across species, impacting cellular functions.
  • This decline is linked to reduced mitochondrial function, stem cell activity, and lifespan in mice.
  • Decreased NAD+ impairs SIRT1 function and the mitochondrial unfolded protein response.

Purpose of the Study:

  • To investigate the role of NAD+ decline in aging.
  • To explore the impact of NAD+ precursors like NMN on age-related cellular dysfunction.
  • To elucidate the relationship between NAD+, DNA damage, and aging.

Main Methods:

  • Supplementation with NAD+ precursors (NR and NMN) in aging mice.
  • Assessment of mitochondrial function, stem cell activity, and lifespan.
Keywords:
DBC1/CCAR2NAD+PARP1SIRT1epigenome

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  • Analysis of NAD+-binding protein DBC1, PARP1 activity, DNA damage, and repair mechanisms.

    • Main Results:

    • NMN supplementation improved mitochondrial and stem cell function and increased lifespan in mice.
    • NAD+ decline leads to DBC1-PARP1 complex formation, inhibiting PARP activity and increasing DNA damage.
    • NMN treatment reduced DBC1-PARP1 complexes, restored PARP activity, and decreased DNA damage in old mice.

    Conclusions:

    • NAD+ levels are critical for maintaining cellular function and DNA repair during aging.
    • The NAD+/SIRT1/PARP1 axis may be a significant factor in aging and lifespan.
    • Restoring NAD+ levels via NMN shows therapeutic potential for age-related decline.