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Study · In vitro (cells) · mouse · 2024

7 results

Nicotinamide Adenine Dinucleotide Precursor Supplementation Modulates Neurite Complexity and Survival in Motor Neurons from Amyotrophic Lateral Sclerosis Models.

Hamilton HL, Akther M, Anis S, Colwell CB, Vargas MR, Pehar M

Antioxidants & redox signaling8 Jul 2024Cited by 4 (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 study7

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

  1. 01LabIn vitro (cells)Mechanism

    In cultured motor neurons from both ALS mouse models, NMN increased neuronal process complexity.

    In plain wordsIn lab tests, NMN increased nerve process complexity in motor neurons from both ALS mouse models.

    Outcome
    IncreaseNeurite complexity in ALS mouse neurons
    Study

    mousen: not reported in source

    cultured motor neurons from TDP-43-overexpressing and hSOD1 G93A ALS mouse models
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN treatment increased the complexity of neuronal processes in motor neurons isolated from both mouse models and in iPSC-derived human motor neurons.
  2. 02LabIn vitro (cells)Mechanism

    In human iPSC-derived motor neurons, NMN increased neuronal process complexity.

    In plain wordsIn cells derived from human stem cells, NMN increased motor neuron process complexity.

    Outcome
    IncreaseNeurite complexity in human motor neurons
    Study

    humann: not reported in source

    human iPSC-derived motor neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN treatment increased the complexity of neuronal processes in motor neurons isolated from both mouse models and in iPSC-derived human motor neurons.
  3. 03LabIn vitro (cells)Mechanism

    In cultured motor neurons, NMN prevented death induced by trophic factor deprivation.

    In plain wordsIn lab tests, NMN prevented motor neuron death after withdrawal of growth support.

    Outcome
    DecreaseTrophic deprivation-induced neuronal death
    Study

    n: not reported in source

    cultured motor neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, NMN prevented neuronal death induced by trophic factor deprivation.
  4. 04LabIn vitro (cells)Mechanism

    In mouse and human motor neurons expressing ALS-linked mutant SOD1, NMN increased glutathione levels.

    In plain wordsIn lab tests, NMN increased glutathione in mouse and human motor neurons with ALS-linked mutant SOD1.

    Outcome
    IncreaseGlutathione in mutant SOD1 motor neurons
    Study

    mouse and humann: not reported in source

    mouse and human motor neurons expressing ALS-linked mutant SOD1
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In mouse and human motor neurons expressing ALS-linked mutant superoxide dismutase 1, NMN induced an increase in glutathione levels, but this effect was not observed in nontransgenic or TDP-43 overexpressing motor neurons.
  5. 05LabIn vitro (cells)Mechanism

    In nontransgenic motor neurons, NMN did not increase glutathione levels.

    In plain wordsIn lab tests, NMN did not increase glutathione in nontransgenic motor neurons.

    Outcome
    No significant changeGlutathione in nontransgenic motor neurons
    Study

    mousen: not reported in source

    nontransgenic motor neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In mouse and human motor neurons expressing ALS-linked mutant superoxide dismutase 1, NMN induced an increase in glutathione levels, but this effect was not observed in nontransgenic or TDP-43 overexpressing motor neurons.
  6. 06LabIn vitro (cells)Mechanism

    In TDP-43-overexpressing motor neurons, NMN did not increase glutathione levels.

    In plain wordsIn lab tests, NMN did not increase glutathione in motor neurons that overexpressed TDP-43.

    Outcome
    No significant changeGlutathione in TDP-43-overexpressing neurons
    Study

    mousen: not reported in source

    TDP-43-overexpressing motor neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In mouse and human motor neurons expressing ALS-linked mutant superoxide dismutase 1, NMN induced an increase in glutathione levels, but this effect was not observed in nontransgenic or TDP-43 overexpressing motor neurons.
  7. 07LabIn vitro (cells)Mechanism

    In cultured motor neurons, NMN normalized cytoplasmic TDP-43 mislocalization induced by overexpression.

    In plain wordsIn lab tests, NMN corrected abnormal TDP-43 location caused by its overexpression.

    Outcome
    DecreaseTDP-43 cytoplasmic mislocalization
    Study

    n: not reported in source

    cultured motor neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In contrast, NMN treatment normalized the TDP-43 cytoplasmic mislocalization induced by its overexpression.

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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