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Study · Animal study (in vivo) · mouse · 2020

3 results

Nicotinamide mononucleotide (NMN) supplementation promotes neurovascular rejuvenation in aged mice: transcriptional footprint of SIRT1 activation, mitochondrial protection, anti-inflammatory, and anti-apoptotic effects.

Kiss T, Nyúl-Tóth Á, Balasubramanian P, Tarantini S, Ahire C, Yabluchanskiy A, Csipo T, Farkas E, Wren JD, Garman L, Csiszar A, Ungvari Z

GeroScience13 Feb 2020Cited by 138 (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 study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In aged mice, NMN restored 204 of 590 age-associated differentially expressed neurovascular genes toward youthful expression levels.

    In plain wordsIn aged mice, NMN restored 204 of 590 altered neurovascular genes toward expression levels in young controls.

    Outcome
    MixedAge-associated neurovascular gene expression
    Study

    mousen: not reported in source

    24-month-old C57BL/6 mice
    Comparator
    Untreated young and aged control mice
    Outcome group
    Aging markers · Nervous system and cognition
    Studied dose
    Dose not stated · 2 weeksAs given in this study (mouse).

    Measurements

    Genes restored toward youthful expression
    204 genes
    NMN-treated aged mice
    Age-associated differentially expressed genes
    590 genes
    aged neurovascular unit

    Source sentences

    Summary
    We identified 590 genes differentially expressed in the aged neurovascular unit, 204 of which are restored toward youthful expression levels by NMN treatment.
    2 context sentences
    Summary · context
    To determine the effects of restoring cellular NAD+ levels on neurovascular gene expression profiles, 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, for 2 weeks.
    Summary · context
    Neurovascular gene expression signatures in NMN-treated aged mice were compared with those in untreated young and aged control mice.

Studies that did not test the peptide alone2

In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

  1. 02Computer modelNot a test of NMN (nicotinamide mononucleotide) aloneIn silicoMechanism

    Analysis of NMN-treated aged mouse neurovascular gene expression indicated SIRT1 activation.

    In plain wordsComputer analysis of aged mouse gene expression indicated SIRT1 activation after NMN treatment.

    Outcome
    IncreaseInferred SIRT1 activation
    Study

    n: not reported in source

    upstream regulator and gene expression analysis
    Comparator
    Untreated young and aged control mice
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    The transcriptional footprint of NMN treatment indicates that increased NAD+ levels promote SIRT1 activation in the neurovascular unit, as demonstrated by analysis of upstream regulators of differentially expressed genes as well as analysis of the expression of known SIRT1-dependent genes.
    2 context sentences
    Summary · context
    To determine the effects of restoring cellular NAD+ levels on neurovascular gene expression profiles, 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, for 2 weeks.
    Summary · context
    Neurovascular gene expression signatures in NMN-treated aged mice were compared with those in untreated young and aged control mice.

    In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

  2. 03Computer modelNot a test of NMN (nicotinamide mononucleotide) aloneIn silicoMechanism

    Pathway analysis predicted mitochondrial rejuvenation, anti-inflammatory, and anti-apoptotic gene pathways as mediators of NMN-associated neurovascular protection.

    In plain wordsComputer analysis predicted that mitochondrial, anti-inflammatory, and anti-apoptotic pathways mediated NMN-associated neurovascular protection.

    Outcome
    Not applicablePredicted neurovascular protective pathways
    Study

    n: not reported in source

    pathway analysis
    Comparator
    Untreated young and aged control mice
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    Pathway analysis predicts that neurovascular protective effects of NMN are mediated by the induction of genes involved in mitochondrial rejuvenation, anti-inflammatory, and anti-apoptotic pathways.
    2 context sentences
    Summary · context
    To determine the effects of restoring cellular NAD+ levels on neurovascular gene expression profiles, 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, for 2 weeks.
    Summary · context
    Neurovascular gene expression signatures in NMN-treated aged mice were compared with those in untreated young and aged control mice.

    In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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