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Nucleotide Excision Repair01:38

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Related Experiment Video

Updated: Apr 20, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
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Linking DNA damage, NAD(+)/SIRT1, and aging.

Leonard Guarente1

  • 1Novartis Professor of Biology, Director of the Glenn Labs for the Science of Aging, and Affiliate of the Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 02139, USA.

Cell Metabolism
|December 3, 2014
PubMed
Summary

DNA damage repair defects cause premature aging. Increasing NAD(+) levels can reverse Sirt1 inactivation and mitochondrial issues in Cockayne Syndrome B, linked to PARP activity.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Defects in DNA damage repair (DDR) pathways are linked to premature aging syndromes.
  • Cockayne Syndrome B (CSB) is a rare genetic disorder characterized by features of premature aging.
  • Nuclear NAD(+) depletion by Poly(ADP-ribose) polymerase (PARP) is implicated in CSB pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic potential of NAD(+) supplementation in CSB.
  • To explore the impact of NAD(+) restoration on Sirt1 activity and mitochondrial function in CSB.

Main Methods:

  • Utilized a mouse model of Cockayne Syndrome B.
  • Administered NAD(+) precursors to CSB mice.
  • Assessed Sirt1 activity, mitochondrial respiration, and markers of aging.

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Main Results:

  • Increased NAD(+) levels in CSB mice reversed Sirt1 inactivation.
  • NAD(+) supplementation ameliorated mitochondrial defects in CSB.
  • Restored mitochondrial function correlated with reduced signs of premature aging.

Conclusions:

  • NAD(+) replenishment is a promising therapeutic strategy for Cockayne Syndrome B.
  • Targeting NAD(+) metabolism may offer a novel approach to treating premature aging disorders associated with DDR defects.