Evidence map›Paper›PMID 29357018›Full record

ReviewNeurochemical research2019

Glutamate Dehydrogenase as a Neuroprotective Target Against Neurodegeneration.

A Young Kim, Eun Joo Baik

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  10. Review
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  12. Creation and gene expression analysis of a giant embryo rice mutant with high GABA content.Molecular breeding : new strategies in plant improvement · 2023
    Article
  13. A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023
    Review
  14. Article
  15. Article
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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.

A Young KimDepartment of Physiology, Ajou University School of Medicine, Suwon, 16499, South Korea.
Eun Joo BaikDepartment of Physiology, Ajou University School of Medicine, Suwon, 16499, South Korea. eunjoo@ajou.ac.kr.
Ajou University · KR

Funding

National Research Foundation of Korea 2012R1A2A01011417National Research Foundation of Korea NRF-2012R1A5A2048183
6 · The paper itself

Abstract

Regulation of glutamate metabolism via glutamate dehydrogenase (GDH) might be the promising therapeutic approach for treating neurodegenerative disorders. In the central nervous system, glutamate functions both as a major excitatory neurotransmitter and as a key intermediate metabolite for neurons. GDH converts glutamate to α-ketoglutarate, which serves as a TCA cycle intermediate. Dysregulated GDH activity in the central nervous system is highly correlated with neurological disorders. Indeed, studies conducted with mutant mice and allosteric drugs have shown that deficient or overexpressed GDH activity in the brain can regulate whole body energy metabolism and affect early onset of Parkinson's disease, Alzheimer's disease, temporal lobe epilepsy, and spinocerebellar atrophy. Moreover, in strokes with excitotoxicity as the main pathophysiology, mice that overexpressed GDH exhibited smaller ischemic lesion than mice with normal GDH expression. In additions, GDH activators improve lesions in vivo by increasing α-ketoglutarate levels. In neurons exposed to an insult in vitro, enhanced GDH activity increases ATP levels. Thus, in an energy crisis, neuronal mitochondrial activity is improved and excitotoxic risk is reduced. Consequently, modulating GDH activity in energy-depleted conditions could be a sound strategy for maintaining the mitochondrial factory in neurons, and thus, protect against metabolic failure.

Indexed as

Adenosine TriphosphateAnimalsDrug Delivery SystemsEnergy MetabolismEnzyme InductionGlutamate DehydrogenaseGlutamic AcidHumansNeurodegenerative DiseasesNeuroprotectionNeuroprotective AgentsAdenosine TriphosphateGlutamate DehydrogenaseGlutamic AcidNeuroprotective AgentsEnergy metabolismGlutamate dehydrogenaseNeurodegenerative disordersNeuroprotection

Identifiers

PMID29357018
OpenAlexW2789218054

What OpenQuestion holds

Textmetadata
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.