Prevention of traumatic brain injury-induced neuron death by intranasal delivery of nicotinamide adenine dinucleotide.

Won SJ, Choi BY, Yoo BH, Sohn M, Ying W, Swanson RA, Suh SW

Journal of neurotrauma17 Apr 2012Cited by 45 (Europe PMC)

PMID22352983PMCIDPMC5972775DOI10.1089/neu.2011.2228PepBankPUB-22352983

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

7 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In rats with TBI, immediate intranasal NAD protected hippocampal CA1 neurons.
In plain wordsIn rats with brain injury, immediate intranasal NAD protected CA1 neurons in the hippocampus.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseCA1 neuronal death
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
The intranasal administration of NAD⁺ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298301
02AnimalAnimal study (in vivo)Efficacy outcome
In rats with TBI, immediate intranasal NAD protected hippocampal CA3 neurons.
In plain wordsIn rats with brain injury, immediate intranasal NAD protected CA3 neurons in the hippocampus.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseCA3 neuronal death
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
The intranasal administration of NAD⁺ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298302
03AnimalAnimal study (in vivo)Efficacy outcome
In rats with TBI, immediate intranasal NAD protected dentate gyrus neurons.
In plain wordsIn rats with brain injury, immediate intranasal NAD protected dentate gyrus neurons in the hippocampus.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseDentate gyrus neuronal death
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
The intranasal administration of NAD⁺ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298303
04AnimalAnimal study (in vivo)Efficacy outcome
In rats with TBI, immediate intranasal NAD did not protect cortical neurons.
In plain wordsIn rats with brain injury, immediate intranasal NAD did not protect cortical neurons.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
No significant changeCortical neuronal death
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
The intranasal administration of NAD⁺ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298304
05AnimalAnimal study (in vivo)Mechanism
In rats with TBI, NAD reduced delayed microglial activation at 7 days after injury.
In plain wordsIn rats with brain injury, NAD reduced microglial activation at 7 days.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMicroglial activation at 7 days
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
In addition, delayed microglial activation normally seen after TBI was reduced by NAD⁺ treatment at 7 days after insult.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298305
06AnimalAnimal study (in vivo)Mechanism
In rats with TBI, NAD did not inhibit neuronal superoxide production after injury.
In plain wordsIn rats with brain injury, NAD did not inhibit neuronal superoxide production.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
No significant changeNeuronal superoxide production
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD⁺ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD⁺ depletion.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298306
07AnimalAnimal study (in vivo)Mechanism
In rats with TBI, NAD did not inhibit PARP-1 accumulation after injury.
In plain wordsIn rats with brain injury, NAD did not inhibit PARP-1 accumulation.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
No significant changePARP-1 accumulation
Study
ratn: not reported in source
Weight-drop traumatic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
20 mg/kg · intranasalAs given in this study (rat).
Source sentences
Summary
Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD⁺ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD⁺ depletion.
1 context sentence(design, population, supporting numbers)
Summary · context
Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death.
Report a problemFND-2235298307

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

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