Evidence map›Paper›PMID 34862742›Full record

ReviewCNS neuroscience & therapeutics2022

Kynurenic acid in neurodegenerative disorders-unique neuroprotection or double-edged sword?

Aleksandra Ostapiuk, Ewa M Urbanska

Open access · goldAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 4 pooled it
5.5field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 4 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. A Single Exercise Session Elicits a Transient Kynurenine Metabolic Signature in Health and Disease: A Systematic Review and Meta-Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  6. PMiScience · 2026
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  7. Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026
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  17. Degradation of the Molecular Basis of Life During the Aging Process.International journal of molecular sciences · 2026
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36 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.

Aleksandra OstapiukLaboratory of Cellular and Molecular Pharmacology, Department of Experimental and Clinical Pharmacology, Medical University of Lublin, Lublin, Poland.
Ewa M UrbanskaLaboratory of Cellular and Molecular Pharmacology, Department of Experimental and Clinical Pharmacology, Medical University of Lublin, Lublin, Poland.ORCID 0000-0002-2704-528X
Medical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe family of kynurenine pathway (KP) metabolites includes compounds produced along two arms of the path and acting in clearly opposite ways. The equilibrium between neurotoxic kynurenines, such as 3-hydroxykynurenine (3-HK) or quinolinic acid (QUIN), and neuroprotective kynurenic acid (KYNA) profoundly impacts the function and survival of neurons. This comprehensive review summarizes accumulated evidence on the role of KYNA in Alzheimer's, Parkinson's and Huntington's diseases, and discusses future directions of potential pharmacological manipulations aimed to modulate brain KYNA. DISCUSSION: The synthesis of specific KP metabolites is tightly regulated and may considerably vary under physiological and pathological conditions. Experimental data consistently imply that shift of the KP to neurotoxic branch producing 3-HK and QUIN formation, with a relative or absolute deficiency of KYNA, is an important factor contributing to neurodegeneration. Targeting specific brain regions to maintain adequate KYNA levels seems vital; however, it requires the development of precise pharmacological tools, allowing to avoid the potential cognitive adverse effects.

conclusionsBoosting KYNA levels, through interference with the KP enzymes or through application of prodrugs/analogs with high bioavailability and potency, is a promising clinical approach. The use of KYNA, alone or in combination with other compounds precisely influencing specific populations of neurons, is awaiting to become a significant therapy for neurodegenerative disorders.

Indexed as

Alzheimer DiseaseAnimalsBrainExcitatory Amino Acid AntagonistsHumansHuntington DiseaseKynurenic AcidKynurenineNeurodegenerative DiseasesNeuronsNeuroprotective AgentsParkinson DiseaseQuinolinic AcidSignal Transduction3-hydroxykynurenineExcitatory Amino Acid AntagonistsKynurenic AcidKynurenineNeuroprotective AgentsQuinolinic AcidAlzheimer's diseaseHuntington's diseasemitochondrial toxinneurodegenerationN-methyl-D-aspartateParkinson's disease

Identifiers

PMID34862742
PMCPMC8673711
OpenAlexW3215089600

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.