Evidence map›Paper›PMID 18789905›Full record

ReviewBrain research2008

Genetic polymorphisms in methyl-group metabolism and epigenetics: lessons from humans and mouse models.

Steven H Zeisel

RetractedOpen access · greenAbstract readReview
In one paragraph

Review in Brain research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Epigenetics and nutritional environmental signals.Integrative and comparative biology · 2014
    Review
  5. Review
  6. One-carbon metabolism factors and leukocyte telomere length.The American journal of clinical nutrition · 2013
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. The effects of dietary choline.Neuroscience bulletin · 2011
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. DNA hypomethylation in the origin and pathogenesis of human diseases.Cellular and molecular life sciences : CMLS · 2009
    Review
  19. Article
  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

1 author at 1 institution in 1 country.

Steven H ZeiselNutrition Research Institute, Department of Nutrition, School of Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. steven_zeisel@unc.edu
University of North Carolina at Chapel Hill · US

Funding

Zonisamide in Patients with Neuropathic Pain Associated with Diabetic NeuropathyM01RR000046 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MUENZER, JOSEPH J. · 1985 to 2008
$38.5M
UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ian Michael Carroll · 1999 to 2026
$31.6M
TIME FRAMES OF CHOLINE ENHANCEMENT OF MEMORYP01AG009525 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF · 1991 to 2010
$11.8M
HUMAN REQUIREMENTS FOR THE NUTRIENT CHOLINER01DK055865 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZEISEL, STEVEN H · 2000 to 2011
$7.6M
NCRR NIH HHS M01 RR000046NCRR NIH HHS RR 00046NIA NIH HHS AG 09525NIA NIH HHS P01 AG009525NIDDK NIH HHS DK 55865NIDDK NIH HHS DK 56350NIDDK NIH HHS P30 DK056350NIDDK NIH HHS R01 DK055865NIEHS NIH HHS ES 10126NIEHS NIH HHS P30 ES010126
6 · The paper itself

Abstract

Choline is an essential nutrient that is critical during fetal brain development. Choline deficiency, through disturbing methyl metabolism, may alter DNA methylation and thereby influence neural precursor cell proliferation and apoptosis. This results in long term alterations in brain structure and function, specifically memory function. A recommended dietary intake for choline in humans was set in 1998, and a portion of the choline requirement can be met via endogenous de novo synthesis of phosphatidylcholine catalyzed by phosphatidylethanolamine N-methyltransferase (PEMT) in the liver. Though many foods contain choline, many humans do not get enough in their diets. When deprived of dietary choline, most adult men and postmenopausal women developed signs of organ dysfunction (fatty liver, liver or muscle cell damage). However, only a portion of premenopausal women developed such problems. The difference in requirement occurs because estrogen induces expression of the PEMT gene and allows premenopausal women to make more of their needed choline endogenously. In addition, there is significant variation in the dietary requirement for choline that can be explained by common genetic variants (single nucleotide polymorphisms; SNPs) in genes of choline and folate metabolism. Some of these increase the risk of choline deficiency many-fold. These variations in choline requirement could have important implications for brain development.

Indexed as

Models, AnimalPolymorphism, GeneticAnimalsCholineEpigenesis, GeneticHumansMetabolic Networks and PathwaysMiceCholine

Identifiers

PMID18789905
PMCPMC2587491
OpenAlexW2002619632

What OpenQuestion holds

Textmetadata
LicenceTDM
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.