Evidence map›Paper›PMID 30192747›Full record

ArticlePLoS genetics2018

Nicotinamide-N-methyltransferase controls behavior, neurodegeneration and lifespan by regulating neuronal autophagy.

Kathrin Schmeisser, J Alex Parker

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Lactate promotes longevity through redox-driven lipid remodeling inbioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
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  10. Review
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  12. The Small-Molecule Enhancers of Autophagy AUTEN-67 and -99 Delay Ageing inInternational journal of molecular sciences · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Mechanisms and inhibitors of nicotinamideRSC medicinal chemistry · 2021
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Kathrin SchmeisserResearch Center of the Centre Hospitalier de l'Université de Montréal (CRCHUM), Department of Neuroscience, Université de Montréal, Quebec, Canada.
J Alex ParkerResearch Center of the Centre Hospitalier de l'Université de Montréal (CRCHUM), Department of Neuroscience, Université de Montréal, Quebec, Canada.ORCID 0000-0002-3333-2445
Centre Hospitalier de l’Université de Montréal · CA

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

Nicotinamide N-methyl-transferase (NNMT) is an essential contributor to various metabolic and epigenetic processes, including the regulating of aging, cellular stress response, and body weight gain. Epidemiological studies show that NNMT is a risk factor for psychiatric diseases like schizophrenia and neurodegeneration, especially Parkinson's disease (PD), but its neuronal mechanisms of action remain obscure. Here, we describe the role of neuronal NNMT using C. elegans. We discovered that ANMT-1, the nematode NNMT ortholog, competes with the methyltransferase LCMT-1 for methyl groups from S-adenosyl methionine. Thereby, it regulates the catalytic capacities of LCMT-1, targeting NPRL-2, a regulator of autophagy. Autophagy is a core cellular, catabolic process for degrading cytoplasmic material, but very little is known about the regulation of autophagy during aging. We report an important role for NNMT in regulation of autophagy during aging, where high neuronal ANMT-1 activity induces autophagy via NPRL-2, which maintains neuronal function in old wild type animals and various disease models, also affecting longevity. In younger animals, however, ANMT-1 activity disturbs neuronal homeostasis and dopamine signaling, causing abnormal behavior. In summary, we provide fundamental insights into neuronal NNMT/ANMT-1 as pivotal regulator of behavior, neurodegeneration, and lifespan by controlling neuronal autophagy, potentially influencing PD and schizophrenia risk in humans.

Indexed as

AnimalsAnimals, Genetically ModifiedAutophagyBehavior, AnimalCaenorhabditis elegansCaenorhabditis elegans ProteinsDisease Models, AnimalDopamineHumansLongevityMethyltransferasesMutagenesis, Site-DirectedNeurodegenerative DiseasesNeuronsNicotinamide N-MethyltransferaseS-AdenosylmethionineANMT-1 protein, C elegansCaenorhabditis elegans ProteinsDopamineMethyltransferasesNicotinamide N-MethyltransferaseS-Adenosylmethionine

Identifiers

PMID30192747
PMCPMC6191153
OpenAlexW2891790842

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.