Evidence map›Paper›PMID 19022981›Full record

ArticleThe Journal of nutrition2008

Arachidonic acid and the brain.

Stanley I Rapoport

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in The Journal of nutrition, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02272010 (Targeted Alterations in n-3 and n-6 Fatty Acids for the Management of Mood Variability in the Maintenance Phase of Bipolar Disorder), which is not on this map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.3field-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.

NCT02272010 nacompletednot on this mapstarted 2014, after this paper: background citation

Targeted Alterations in n-3 and n-6 Fatty Acids for the Management of Mood Variability in the Maintenance Phase of Bipolar Disorder

TypeinterventionalSponsorMilton S. Hershey Medical CenterRan2014 to 2019Enrolled83ConditionsBipolar DisorderArmsExperimental Diet, Comparator Diet
3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 153 citations in OpenAlex.

  1. Trial
  2. MaternalNutrients · 2026
    Review
  3. Pharmaceutics · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Arachidonic Acid Mobilization and Peroxidation Promote Microglial Dysfunction in Aβ Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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.

Stanley I RapoportBrain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. sir@helix.nih.gov
National Institutes of Health · US

Funding

Lipid Nutrition and the BrainZIAAG000399 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2009 to 2014
$3.7M
Lipid Nutrition and the BrainZ01AG000399 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2005 to 2008
$1.2M
Intramural NIH HHS
6 · The paper itself

Abstract

Kinetic methods in unanesthetized rodents have shown that turnover rates of arachidonic acid (AA) and docosahexaenoic acid (DHA) in brain membrane phospholipids are rapid and energy consuming and that phospholipase A(2) (PLA(2)) and acyl-CoA synthetase enzymes that regulate turnover are specific for one or the other PUFA. Thus, AA turnover in brain phospholipids was reduced, and AA-selective cytosolic cPLA(2) or acyl-CoA synthetase, as well as cyclooxygenase (COX)-2, were downregulated in brains of rats given drugs effective against bipolar disorder, whereas DHA turnover and expression of DHA-selective calcium-independent iPLA(2) were unchanged. Additionally, the brain AA and DHA cascades can be altered reciprocally by dietary or genetic conditions. Thus, following 15 wk of dietary (n-3) PUFA deprivation, DHA loss from rat brain was slowed because of reduced iPLA(2) and COX-1 expression, whereas AA-selective cPLA(2), sPLA(2), and COX-2 were upregulated, as were AA and docosapentaenoic acid concentrations. Measured rates of AA and DHA incorporation into brain represent their respective rates of metabolic consumption, because these PUFA are not synthesized de novo or converted significantly from their precursors in brain. In healthy human volunteers, positron emission tomography (PET) was used to show that the brain consumes AA and DHA at respective rates of 17.8 and 4.6 mg/d, whereas in patients with Alzheimer disease, AA consumption is elevated. In the future, PET could be used to relate human brain rates of AA and DHA consumption to liver PUFA metabolism and dietary PUFA intake.

Indexed as

AnimalsAntimanic AgentsArachidonic AcidBrainDocosahexaenoic AcidsFatty Acids, Omega-3HumansKineticsLithiumModels, NeurologicalPhospholipases A2Positron-Emission TomographyRatsUp-RegulationAntimanic AgentsArachidonic AcidDocosahexaenoic AcidsFatty Acids, Omega-3LithiumPhospholipases A2

Identifiers

PMID19022981
PMCPMC3415870
OpenAlexW2133285177

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.