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Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage.

Yuri LeeHyeseon JeongKyung Hwan ParkKyung Won Kim
Published in: Biomolecules (2020)
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.
Keyphrases
  • cerebral ischemia
  • living cells
  • stem cells
  • spinal cord injury
  • fluorescent probe
  • brain injury
  • subarachnoid hemorrhage
  • single molecule
  • optical coherence tomography
  • wound healing