Deletion of CD38 and supplementation of NAD⁺ attenuate axon degeneration in a mouse facial nerve axotomy model.

Takaso Y, Noda M, Hattori T, Roboon J, Hatano M, Sugimoto H, Brenner C, Yamamoto Y, Okamoto H, Higashida H, Ito M, Yoshizaki T, Hori O

Scientific reports20 Oct 2020Cited by 15 (Europe PMC)

PMID33082370PMCIDPMC7576594DOI10.1038/s41598-020-73984-3PepBankPUB-33082370

Download PDF PubMedAsk about this study

Jump to 8 results

Summary

Following facial nerve axotomy, nerve function is not fully restored even after reconstruction. This may be attributed to axon degeneration/neuronal death and sustained neuroinflammation. CD38 is an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD⁺) and is a candidate molecule for regulating neurodegeneration and neuroinflammation. In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice. Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different. In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy. Supplementation of NAD⁺ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy. These results suggest that CD38 deletion and supplementation of NAD⁺ may protect transected axon cell-autonomously after facial nerve axotomy.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study8

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone8

In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

01AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after facial nerve axotomy, deletion of the NAD+-hydrolyzing enzyme CD38 reduced microglial activation versus wild-type mice.
In plain wordsIn mice after axotomy, deletion of the NAD+-hydrolyzing enzyme CD38 reduced microglial activation compared with wild-type mice.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMicroglial activation
Study
mousen: not reported in source
Facial nerve axotomy
Comparator
Wild-type mice
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237001
02AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after facial nerve axotomy, deletion of the NAD+-hydrolyzing enzyme CD38 did not significantly change neuronal death versus wild-type mice.
In plain wordsIn mice after axotomy, deletion of the NAD+-hydrolyzing enzyme CD38 did not significantly change neuronal death compared with wild-type mice.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
No significant changeNeuronal death
Study
mousen: not reported in source
Facial nerve axotomy
Comparator
Wild-type mice
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237002
03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, CD38 deletion delayed axon degeneration compared with wild-type mice.
In plain wordsIn mice after axotomy, CD38 deletion delayed axon degeneration compared with wild-type mice.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseAxon degeneration after CD38 deletion
Study
mousen: not reported in source
Facial nerve axotomy
Comparator
Wild-type mice
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy.
2 context sentences(design, population, supporting numbers)
Summary · context
Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different.
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237003
04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, CD38 deletion delayed demyelination compared with wild-type mice.
In plain wordsIn mice after axotomy, CD38 deletion delayed demyelination compared with wild-type mice.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseDemyelination after CD38 deletion
Study
mousen: not reported in source
Facial nerve axotomy
Comparator
Wild-type mice
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy.
2 context sentences(design, population, supporting numbers)
Summary · context
Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different.
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237004
05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, CD38 deletion reduced facial nerve macrophage accumulation compared with wild-type mice.
In plain wordsIn mice after axotomy, CD38 deletion reduced facial nerve macrophage accumulation compared with wild-type mice.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMacrophage accumulation after CD38 deletion
Study
mousen: not reported in source
Facial nerve axotomy
Comparator
Wild-type mice
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy.
2 context sentences(design, population, supporting numbers)
Summary · context
Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different.
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237005
06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, NAD+ supplementation with NR slowed axon degeneration.
In plain wordsIn mice after axotomy, the NAD+ precursor NR slowed axon degeneration.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseAxon degeneration after NR
Study
mousen: not reported in source
Facial nerve axotomy
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Supplementation of NAD⁺ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237006
07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, NAD+ supplementation with NR slowed demyelination.
In plain wordsIn mice after axotomy, the NAD+ precursor NR slowed demyelination.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseDemyelination after NR
Study
mousen: not reported in source
Facial nerve axotomy
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Supplementation of NAD⁺ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237007
08AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice after axotomy, NAD+ supplementation with NR did not alter macrophage infiltration.
In plain wordsIn mice after axotomy, the NAD+ precursor NR did not change macrophage infiltration.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Direction not reportedMacrophage infiltration after NR
Study
mousen: not reported in source
Facial nerve axotomy
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
Supplementation of NAD⁺ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we analyzed the effect of CD38 deletion and NAD⁺ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3308237008

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
14 Oct 2026, 05:02 UTC
Study results updated
Version 1
14 Oct 2026, 01:46 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

MeSH terms

PepBank is a research reference. Talk to a doctor before you use any peptide.