Evidence map›Paper›PMID 32792905›Full record

ReviewFrontiers in neuroscience2020

The Redox Biology of Excitotoxic Processes: The NMDA Receptor, TOPA Quinone, and the Oxidative Liberation of Intracellular Zinc.

Elias Aizenman, Ralph H Loring, Ian J Reynolds, Paul A Rosenberg

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. A soybean based-diet prevents Cadmium access to rat cerebellum, maintaining trace elements homeostasis and avoiding morphological alterations.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
    Article
  5. Review
  6. The ZIP3 Zinc Transporter Is Localized to Mossy Fiber Terminals and Is Required for Kainate-Induced Degeneration of CA3 Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Article
  8. Article
  9. Zinc in the Brain: Friend or Foe?International journal of molecular sciences · 2020
    Review
  10. A NeurotoxicFrontiers in molecular neuroscience · 2020
    Review
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 3 institutions in 1 country.

Elias AizenmanDepartment of Neurobiology, Pittsburgh Institute for Neurodegenerative Diseases, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Ralph H LoringDepartment of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, Boston, MA, United States.
Ian J ReynoldsRewind Therapeutics, Leuven, Belgium.
Paul A RosenbergProgram in Neuroscience, F.M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.
Boston Children's Hospital · USNortheastern University · USUniversity of Pittsburgh · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Liberation of Intracellular Zinc and Neuronal Cell DeathR01NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2002 to 2022
$8.2M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
An interneuronal signaling network governs the fate of retinal ganglion cells after optic nerve injuryR01EY027881 · NEI · BOSTON CHILDREN'S HOSPITAL · PI ROSENBERG, PAUL ALLEN · 2018 to 2022
$3.5M
Liberation of Intracellular Zinc and Neuronal Cell DeathR56NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2007 to 2007
$371k
NEI NIH HHS R01 EY027881NICHD NIH HHS P30 HD018655NICHD NIH HHS U54 HD090255NINDS NIH HHS R01 NS043277NINDS NIH HHS R56 NS043277
6 · The paper itself

Abstract

This special issue of Frontiers in Neuroscience-Neurodegeneration celebrates the 50th anniversary of John Olney's seminal work introducing the concept of excitotoxicity as a mechanism for neuronal cell death. Since that time, fundamental research on the pathophysiological activation of glutamate receptors has played a central role in our understanding of excitotoxic cellular signaling pathways, leading to the discovery of many potential therapeutic targets in the treatment of acute or chronic/progressive neurodegenerative disorders. Importantly, excitotoxic signaling processes have been found repeatedly to be closely intertwined with oxidative cellular cascades. With this in mind, this review looks back at long-standing collaborative efforts by the authors linking cellular redox status and glutamate neurotoxicity, focusing first on the discovery of the redox modulatory site of the

Indexed as

catecholamineexcitotoxicityNMDA receptorpotassium channelredoxzinc

Identifiers

PMID32792905
PMCPMC7393236
OpenAlexW3045030047

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.