Evidence map›Paper›PMID 24421768›Full record

ReviewFrontiers in neuroenergetics2013

N-Acetylaspartate reductions in brain injury: impact on post-injury neuroenergetics, lipid synthesis, and protein acetylation.

John R Moffett, Peethambaran Arun, Prasanth S Ariyannur, Aryan M A Namboodiri

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in neuroenergetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 3 pooled it
5.2field-weighted citation impact, top 4% 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

107 citing papers in PubMed, 3 syntheses or guidelines pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Toxic Effects of Glyphosate on the Nervous System: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  4. Effects of the SGLT2 inhibitor dapagliflozin in early Alzheimer's disease: A randomized controlled trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Trial
  5. Trial
  6. Trial
  7. Metabolite ratiomics: Rapid diagnosis and classification of gliomas for intraoperative application during brain surgery.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Frontiers in neuroscience · 2026
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

47 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

4 authors at 1 institution in 1 country.

John R MoffettNeuroscience Program, Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences Bethesda, MD, USA.
Peethambaran ArunNeuroscience Program, Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences Bethesda, MD, USA.
Prasanth S AriyannurNeuroscience Program, Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences Bethesda, MD, USA.
Aryan M A NamboodiriNeuroscience Program, Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences Bethesda, MD, USA.
Uniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-Acetylaspartate (NAA) is employed as a non-invasive marker for neuronal health using proton magnetic resonance spectroscopy (MRS). This utility is afforded by the fact that NAA is one of the most concentrated brain metabolites and that it produces the largest peak in MRS scans of the healthy human brain. NAA levels in the brain are reduced proportionately to the degree of tissue damage after traumatic brain injury (TBI) and the reductions parallel the reductions in ATP levels. Because NAA is the most concentrated acetylated metabolite in the brain, we have hypothesized that NAA acts in part as an extensive reservoir of acetate for acetyl coenzyme A synthesis. Therefore, the loss of NAA after TBI impairs acetyl coenzyme A dependent functions including energy derivation, lipid synthesis, and protein acetylation reactions in distinct ways in different cell populations. The enzymes involved in synthesizing and metabolizing NAA are predominantly expressed in neurons and oligodendrocytes, respectively, and therefore some proportion of NAA must be transferred between cell types before the acetate can be liberated, converted to acetyl coenzyme A and utilized. Studies have indicated that glucose metabolism in neurons is reduced, but that acetate metabolism in astrocytes is increased following TBI, possibly reflecting an increased role for non-glucose energy sources in response to injury. NAA can provide additional acetate for intercellular metabolite trafficking to maintain acetyl CoA levels after injury. Here we explore changes in NAA, acetate, and acetyl coenzyme A metabolism in response to brain injury.

Indexed as

acetyl coenzyme Aacetyl coenzyme A synthaseaspartoacylasemitochondriaNAA

Identifiers

PMID24421768
PMCPMC3872778
OpenAlexW1965336960

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.