Evidence map›Paper›PMID 21293295›Full record

ReviewJournal of neuropathology and experimental neurology2011

Neuronal-astrocyte metabolic interactions: understanding the transition into abnormal astrocytoma metabolism.

Dennis A Turner, David Cory Adamson

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Astrocytic PYGM attenuates tau pathology by promoting lactate-mediated neuroprotection.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Glioma neuron symbiosis: a hypothesis.Frontiers in neuroscience · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024
    Review
  19. Review
  20. Article

26 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

2 authors at 1 institution in 1 country.

Dennis A TurnerNeurosurgery and Neurobiology, Duke University Medical Center, and Research and Surgery Services, Durham VAMC, Durham, NC 27710, USA. dennis.turner@duke.edu
David Cory Adamson
Duke University · US

Funding

Lifespan Metabolic Neuroprotection during HypoglycemiaR01NS051856 · NINDS · DUKE UNIVERSITY · PI TURNER, DENNIS ALAN · 2004 to 2008
$1.7M
Neuronal Fatigue in Aging Hippocampus during Sustained Metabolic DemandR01AG037599 · NIA · DUKE UNIVERSITY · PI TURNER, DENNIS ALAN · 2010 to 2013
$1.1M
NIA NIH HHS R01 AG037599NINDS NIH HHS R01 NS051856
6 · The paper itself

Abstract

Brain function depends on complex metabolic interactions among only a few different cell types, with astrocytes providing critical support for neurons. Astrocyte functions include buffering the extracellular space, providing substrates to neurons, interchanging glutamate and glutamine for synaptic transmission with neurons, and facilitating access to blood vessels. Whereas neurons possess highly oxidative metabolism and easily succumb to ischemia, astrocytes rely more on glycolytic metabolism and hence are less susceptible tolack of oxygen. Astrocytoma cells seem to retain basic metabolic mechanisms of astrocytes; for example, they show a high glycolytic rate, lactate extrusion, ability to flourish under hypoxia, and opportunistic use of mechanisms to enhance cell division and maintain growth. Differences in metabolism between neurons and astrocytes may also extend to astrocytoma cells, providing therapeutic opportunities against astrocytomas, including sensitivity to acetate, a high rate of glycolysis and lactate extrusion, glutamate uptake transporters, differential sensitivities of monocarboxylate transporters, presence of glycogen, high interlinking with gap junctions, use of nicotinamide adenine dinucleotide phosphate for lipid synthesis, using different isoforms of synthetic enzymes (e.g. isocitrate dehydrogenase, pyruvate carboxylase, pyruvate kinase, lactate dehydrogenase), and different glucose uptake mechanisms. These unique metabolic susceptibilities may augment conventional therapeutic attacks based on cell division differences and surface receptors alone.

Indexed as

AcetatesAnimalsAstrocytesAstrocytomaBlood VesselsEndothelium, VascularEnergy MetabolismGlutamic AcidHumansNeuronsAcetatesGlutamic Acid

Identifiers

PMID21293295
PMCPMC3045672
OpenAlexW2028768218

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.