Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage

Biomolecules. 2020 Jul 2;10(7):993. doi: 10.3390/biom10070993.


Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor that mediates numerous biological processes in all living cells. Multiple NAD+ biosynthetic enzymes and NAD+-consuming enzymes are involved in neuroprotection and axon regeneration. The nematode Caenorhabditis elegans has served as a model to study the neuronal role of NAD+ because many molecular components regulating NAD+ are highly conserved. This review focuses on recent findings using C. elegans models of neuronal damage pertaining to the neuronal functions of NAD+ and its precursors, including a neuroprotective role against excitotoxicity and axon degeneration as well as an inhibitory role in axon regeneration. The regulation of NAD+ levels could be a promising therapeutic strategy to counter many neurodegenerative diseases, as well as neurotoxin-induced and traumatic neuronal damage.

Keywords: C. elegans; NAD+; NMAT-2; Nmnat; PARP; axon regeneration; neuroprotection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Caenorhabditis elegans
  • Disease Models, Animal
  • NAD / pharmacology
  • NAD / therapeutic use*
  • Nerve Regeneration / drug effects
  • Neurodegenerative Diseases / drug therapy*
  • Neurodegenerative Diseases / etiology
  • Neurodegenerative Diseases / metabolism
  • Neuroprotection
  • Neurotoxins / toxicity*
  • Signal Transduction


  • Neurotoxins
  • NAD