NAD⁺ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair.

Fang EF, Kassahun H, Croteau DL, Scheibye-Knudsen M, Marosi K, Lu H, Shamanna RA, Kalyanasundaram S, Bollineni RC, Wilson MA, Iser WB, Wollman BN and 10 more

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Morevati M, Li J, Kerr JS, Lu Q, Waltz TB, Tian J, Sinclair DA, Mattson MP, Nilsen H, Bohr VA

Cell metabolism1 Oct 2016Cited by 505 (Europe PMC)

PMID27732836PMCIDPMC5777858DOI10.1016/j.cmet.2016.09.004PepBankPUB-27732836

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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 study9

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

Studies that did not test the peptide alone9

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 mouse and worm A-T models, NAD+-replenishing treatments reduced neuropathology severity.
In plain wordsIn mice and worms with A-T models, treatments that replenished NAD+ reduced nerve disease severity.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseA-T neuropathology severity
Study
mice and wormsn: not reported in source
ATM-deficient ataxia telangiectasia models
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Treatments that replenish intracellular NAD⁺ reduce the severity of A-T neuropathology, normalize neuromuscular function, delay memory loss, and extend lifespan in both animal models.
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).
Report a problemFND-2773283602
02AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mouse and worm A-T models, NAD+-replenishing treatments normalized neuromuscular function.
In plain wordsIn mice and worms with A-T models, treatments that replenished NAD+ normalized nerve and muscle function.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseNeuromuscular function
Study
mice and wormsn: not reported in source
ATM-deficient ataxia telangiectasia models
Outcome group
Exercise and physical function · Musculoskeletal
Source sentences
Summary
Treatments that replenish intracellular NAD⁺ reduce the severity of A-T neuropathology, normalize neuromuscular function, delay memory loss, and extend lifespan in both animal models.
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).
Report a problemFND-2773283603
03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mouse and worm A-T models, NAD+-replenishing treatments delayed memory loss.
In plain wordsIn mice and worms with A-T models, treatments that replenished NAD+ delayed memory loss.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMemory loss
Study
mice and wormsn: not reported in source
ATM-deficient ataxia telangiectasia models
Outcome group
Cognition and memory · Nervous system and cognition
Source sentences
Summary
Treatments that replenish intracellular NAD⁺ reduce the severity of A-T neuropathology, normalize neuromuscular function, delay memory loss, and extend lifespan in both animal models.
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).
Report a problemFND-2773283604
04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mouse and worm A-T models, NAD+-replenishing treatments extended lifespan.
In plain wordsIn mice and worms with A-T models, treatments that replenished NAD+ extended lifespan.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseLifespan
Study
mice and wormsn: not reported in source
ATM-deficient ataxia telangiectasia models
Outcome group
Mortality · Aging and longevity
Source sentences
Summary
Treatments that replenish intracellular NAD⁺ reduce the severity of A-T neuropathology, normalize neuromuscular function, delay memory loss, and extend lifespan in both animal models.
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).
Report a problemFND-2773283605
05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designOther
In ATM-deficient neurons, mice, and worms, the study reported low NAD+.
In plain wordsIn ATM-deficient neurons, mice, and worms, natural NAD+ levels were low.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseLow intracellular NAD+
Study
mice and wormsn: not reported in source
ATM-deficient neurons, mice, and worms
Outcome group
Mitochondrial function · Whole body
Source sentences
Summary
Here we report and examine the significance of increased PARylation, low NAD⁺, and mitochondrial dysfunction in ATM-deficient neurons, mice, and worms.
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).
Report a problemFND-2773283601
06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ATM-deficient neurons, mice, and worms, the study reported increased PARylation alongside low NAD+.
In plain wordsIn ATM-deficient neurons, mice, and worms, PARylation increased alongside low NAD+.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseIncreased PARylation in ATM-deficient models
Study
mice and wormsn: not reported in source
ATM-deficient neurons, mice, and worms
Outcome group
Receptor activity and mechanism · Whole body
Source sentences
Summary
Here we report and examine the significance of increased PARylation, low NAD⁺, and mitochondrial dysfunction in ATM-deficient neurons, mice, and worms.
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).
Report a problemFND-2773283608
07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ATM-deficient neurons, mice, and worms, the study reported mitochondrial dysfunction alongside low NAD+.
In plain wordsIn ATM-deficient neurons, mice, and worms, mitochondria had dysfunction alongside low NAD+.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Direction not reportedMitochondrial dysfunction in ATM-deficient models
Study
mice and wormsn: not reported in source
ATM-deficient neurons, mice, and worms
Outcome group
Mitochondrial function · Whole body
Source sentences
Summary
Here we report and examine the significance of increased PARylation, low NAD⁺, and mitochondrial dysfunction in ATM-deficient neurons, mice, and worms.
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).
Report a problemFND-2773283609
08LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In neurons, treatments that increased intracellular NAD+ stimulated DNA repair.
In plain wordsIn lab tests, treatments that increased intracellular NAD+ stimulated DNA repair in neurons.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseNeuronal DNA repair
Study
n: not reported in source
neurons
Outcome group
Aging markers · Nervous system and cognition
Source sentences
Summary
Mechanistically, treatments that increase intracellular NAD⁺ also stimulate neuronal DNA repair and improve mitochondrial quality via mitophagy.
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).
Report a problemFND-2773283606
09LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In A-T models, treatments that increased intracellular NAD+ improved mitochondrial quality via mitophagy.
In plain wordsIn lab tests, treatments that increased intracellular NAD+ improved mitochondrial quality through mitophagy.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseMitochondrial quality via mitophagy
Study
n: not reported in source
Outcome group
Mitochondrial function · Nervous system and cognition
Source sentences
Summary
Mechanistically, treatments that increase intracellular NAD⁺ also stimulate neuronal DNA repair and improve mitochondrial quality via mitophagy.
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).
Report a problemFND-2773283607

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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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