Evidence map›Paper›PMID 27031963›Full record

ArticleCell death & disease2016

Parp mutations protect against mitochondrial dysfunction and neurodegeneration in a PARKIN model of Parkinson's disease.

S Lehmann, A C Costa, I Celardo, S H Y Loh, L M Martins

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 66 citations in OpenAlex.

  1. A combined artificial intelligence-wet lab approach identifies a pivotal role of the NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026
    Review
  3. HM568 Enhances NADMolecular neurobiology · 2026
    Article
  4. Article
  5. The role of NADnpj metabolic health and disease · 2025
    Review
  6. Review
  7. Article
  8. Autophagy-NADFrontiers in molecular biosciences · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Nicotinamide Adenine Dinucleotide (NADAntioxidants & redox signaling · 2023
    Review
  13. Review
  14. Article
  15. DNA Damage-Mediated Neurotoxicity in Parkinson's Disease.International journal of molecular sciences · 2023
    Review
  16. Muscle PARP1 inhibition extends lifespan through AMPKα PARylation and activation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Balancing NADCellular and molecular life sciences : CMLS · 2022
    Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

S LehmannCell Death Regulation Laboratory, MRC Toxicology Unit, Lancaster Road, Leicester LE1 9HN, UK.
A C CostaCell Death Regulation Laboratory, MRC Toxicology Unit, Lancaster Road, Leicester LE1 9HN, UK.
I CelardoCell Death Regulation Laboratory, MRC Toxicology Unit, Lancaster Road, Leicester LE1 9HN, UK.
S H Y LohCell Death Regulation Laboratory, MRC Toxicology Unit, Lancaster Road, Leicester LE1 9HN, UK.
L M MartinsCell Death Regulation Laboratory, MRC Toxicology Unit, Lancaster Road, Leicester LE1 9HN, UK.
MRC Toxicology Unit · GB

Funding

Medical Research Council MC_U132674518
6 · The paper itself

Abstract

The co-enzyme nicotinamide adenine dinucleotide (NAD(+)) is an essential co-factor for cellular energy generation in mitochondria as well as for DNA repair mechanisms in the cell nucleus involving NAD(+)-consuming poly (ADP-ribose) polymerases (PARPs). Mitochondrial function is compromised in animal models of Parkinson's disease (PD) associated with PARKIN mutations. Here, we uncovered alterations in NAD(+) salvage metabolism in Drosophila parkin mutants. We show that a dietary supplementation with the NAD(+) precursor nicotinamide rescues mitochondrial function and is neuroprotective. Further, by mutating Parp in parkin mutants, we show that this increases levels of NAD(+) and its salvage metabolites. This also rescues mitochondrial function and suppresses dopaminergic neurodegeneration. We conclude that strategies to enhance NAD(+) levels by administration of dietary precursors or the inhibition of NAD(+)-dependent enzymes, such as PARP, that compete with mitochondria for NAD(+) could be used to delay neuronal death associated with mitochondrial dysfunction.

Indexed as

AnimalsBlotting, WesternBrainDietary SupplementsDisease Models, AnimalDopaminergic NeuronsDrosophilaDrosophila ProteinsGenotypeLongevityMaleMembrane Potential, MitochondrialMitochondriaMutagenesisNADNiacinamideDrosophila ProteinsNADNiacinamideparkin proteinPoly(ADP-ribose) PolymerasesUbiquitin-Protein Ligases

Identifiers

PMID27031963
PMCPMC4823968
OpenAlexW2322530366

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.