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Study · Measured the body's own peptide · 2021

16 results

NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING.

Hou Y, Wei Y, Lautrup S, Yang B, Wang Y, Cordonnier S, Mattson MP, Croteau DL, Bohr VA

Proceedings of the National Academy of Sciences of the United States of America1 Sept 2021Cited by 459 (Europe PMC)

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 study16

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

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Other

    In APP/PS1 mutant mice, natural brain NAD+ levels were reduced.

    In plain wordsIn mice, natural brain NAD+ levels were reduced.

    Outcome
    DecreaseBrain NAD+ levels
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    Here, we report that levels of NAD+ are reduced and markers of inflammation increased in the brains of APP/PS1 mutant transgenic mice with beta-amyloid pathology.

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Other

    In APP/PS1 mutant mice, NR treatment increased brain NAD+ levels.

    In plain wordsIn mice, NR increased natural brain NAD+ levels.

    Outcome
    IncreaseBrain NAD+ after NR
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone14

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).

  1. 03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In APP/PS1 mutant mice, the NAD+ precursor NR reduced proinflammatory cytokine expression.

    In plain wordsIn mice, the NAD+ precursor NR reduced inflammatory cytokine expression.

    Outcome
    DecreaseProinflammatory cytokine expression
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.

    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).

  2. 04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In APP/PS1 mutant mice, the NAD+ precursor NR decreased microglial activation.

    In plain wordsIn mice, the NAD+ precursor NR decreased microglial activation.

    Outcome
    DecreaseMicroglial activation
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Inflammation markers · Nervous system and cognition

    Source sentences

    Summary
    Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.

    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).

  3. 05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In APP/PS1 mutant mice, the NAD+ precursor NR decreased astrocyte activation.

    In plain wordsIn mice, the NAD+ precursor NR decreased astrocyte activation.

    Outcome
    DecreaseAstrocyte activation
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Inflammation markers · Nervous system and cognition

    Source sentences

    Summary
    Treatment of APP/PS1 mutant mice with the NAD+ precursor nicotinamide riboside (NR) for 5 mo increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.

    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).

  4. 06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In AD mouse brains, the NAD+ precursor NR reduced NLRP3 inflammasome expression.

    In plain wordsIn mice, the NAD+ precursor NR reduced NLRP3 inflammasome expression.

    Outcome
    DecreaseNLRP3 inflammasome expression
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Inflammation markers · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.

    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).

  5. 07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In AD mouse brains, the NAD+ precursor NR reduced DNA damage.

    In plain wordsIn mice, the NAD+ precursor NR reduced brain DNA damage.

    Outcome
    DecreaseDNA damage
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Aging markers · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.

    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).

  6. 08AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In AD mouse brains, the NAD+ precursor NR reduced apoptosis.

    In plain wordsIn mice, the NAD+ precursor NR reduced brain cell death.

    Outcome
    DecreaseApoptosis
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.

    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).

  7. 09AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In AD mouse brains, the NAD+ precursor NR reduced cellular senescence.

    In plain wordsIn mice, the NAD+ precursor NR reduced brain cellular senescence.

    Outcome
    DecreaseCellular senescence
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Aging markers · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.

    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).

  8. 10AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In AD mice, the NAD+ precursor NR normalized elevated cGAS-STING.

    In plain wordsIn mice, the NAD+ precursor NR normalized elevated cGAS-STING.

    Outcome
    DecreasecGAS-STING elevation
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    cGAS-STING elevation was observed in the AD mice and normalized by NR treatment.

    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).

  9. 11AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In APP/PS1 mutant mice, the NAD+ precursor NR reduced elevated cytoplasmic DNA.

    In plain wordsIn mice, the NAD+ precursor NR reduced elevated cytoplasmic DNA.

    Outcome
    DecreaseCytoplasmic DNA
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Aging markers · Nervous system and cognition

    Source sentences

    Summary
    Levels of ectopic (cytoplasmic) DNA were increased in APP/PS1 mutant mice and human AD fibroblasts and down-regulated by NR.

    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).

  10. 12AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In APP/PS1 mutant mice, the NAD+ precursor NR induced mitophagy.

    In plain wordsIn mice, the NAD+ precursor NR induced mitophagy.

    Outcome
    IncreaseMitophagy
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    NR treatment induced mitophagy and improved cognitive and synaptic functions in APP/PS1 mutant 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).

  11. 13AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In APP/PS1 mutant mice, the NAD+ precursor NR improved cognitive function.

    In plain wordsIn mice, the NAD+ precursor NR improved cognitive function.

    Outcome
    IncreaseCognitive function
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Cognition and memory · Nervous system and cognition

    Source sentences

    Summary
    NR treatment induced mitophagy and improved cognitive and synaptic functions in APP/PS1 mutant 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).

  12. 14AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In APP/PS1 mutant mice, the NAD+ precursor NR improved synaptic function.

    In plain wordsIn mice, the NAD+ precursor NR improved synaptic function.

    Outcome
    IncreaseSynaptic function
    Study

    mousen: not reported in source

    APP/PS1 mutant transgenic mice
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    NR treatment induced mitophagy and improved cognitive and synaptic functions in APP/PS1 mutant 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).

  13. 15LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism

    In cultured microglia, NR benefits were suggested to depend partly on cGAS-STING signaling associated with NAD+ depletion.

    In plain wordsIn cells, benefits of the NAD+ precursor NR appeared partly dependent on cGAS-STING signaling.

    Outcome
    Not applicablecGAS-STING-dependent pathway
    Study

    n: not reported in source

    Microglia culture
    Outcome group
    Receptor activity and mechanism · Immune and inflammation

    Source sentences

    Summary
    Cell culture experiments using microglia suggested that the beneficial effects of NR are, in part, through a cGAS-STING-dependent pathway.

    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).

  14. 16LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism

    In human AD fibroblasts, the NAD+ precursor NR reduced elevated cytoplasmic DNA.

    In plain wordsIn AD fibroblast cells, the NAD+ precursor NR reduced elevated cytoplasmic DNA.

    Outcome
    DecreaseCytoplasmic DNA
    Study

    humann: not reported in source

    AD fibroblasts
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    Levels of ectopic (cytoplasmic) DNA were increased in APP/PS1 mutant mice and human AD fibroblasts and down-regulated by NR.

    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).

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.

  1. Version 2Current

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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