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Effects of NAD(+) in Caenorhabditis elegans Models of Neuronal Damage

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...

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Detalles Bibliográficos
Autores principales: Lee, Yuri, Jeong, Hyeseon, Park, Kyung Hwan, Kim, Kyung Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407593/
https://www.ncbi.nlm.nih.gov/pubmed/32630651
http://dx.doi.org/10.3390/biom10070993
Descripción
Sumario: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.