ArticleInternational journal of tryptophan research : IJTR2012
Quinolinic Acid, an endogenous molecule combining excitotoxicity, oxidative stress and other toxic mechanisms.
Article in International journal of tryptophan research : IJTR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- Potential biomarkers for tuberculous meningitis diagnosis using metabolomics and proteomics: a systematic review.BMC infectious diseases · 2025Pooled it
- Changes in Mood and Tryptophan Metabolism Following a 12-Week Endurance Exercise Combined with Time-Restricted Eating in Healthy Adults.Nutrients · 2026Trial
- Linking protein misfolding and heat stress: a common role for the kynurenine pathway.Metabolic brain disease · 2026Review
- The role of the kynurenine pathway in the pathogenesis of pain and affective disorders after traumatic brain injury.Brain, behavior, & immunity - health · 2026Review
- Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- L-carnitine modulates molecular responses associated with inflammation, endoplasmic reticulum stress, and neurotrophic signaling in cerebral cortex of neonatal GcdhMetabolic brain disease · 2026Article
- Gestational kynurenine metabolites mediate effects of pregnancy adiposity on child negative affect.Journal of child psychology and psychiatry, and allied disciplines · 2026Article
- A metabolic constraint in de novo NAD+ synthesis drives mucosal inflammation in IBD.Journal of Crohn's & colitis · 2026Article
- Kynurenine Pathway, Nrf2 and NF-κB Cross-Regulation in the CNS: An Overview.Molecular neurobiology · 2026Review
- Physical Activity, Metabolic Dysfunction, and the Kynurenine Pathway in Endometriosis and Polycystic Ovary Syndrome: A Literature Review.Biomolecules · 2026Review
- Article
- Glutamate Receptor Agonists as Triggers of Neurotoxicity: Decoding Pathways of Five Neurotoxins and Potential Therapeutic Targets.ACS omega · 2026Review
- Glucocorticoid Treatment Dampens Kynurenine Pathway Activation and Cytokine Release in Immune Stimulated Human Microglia.International journal of tryptophan research : IJTR · 2026Article
- Targeting the microbiota-gut-brain axis in post-stroke insomnia: a phase-dependent therapeutic framework.Frontiers in neuroscience · 2026Review
- Anandamide-Induced Neuroprotection of Cortical Neurons Relies on Metabolic/Redox Regulation and Mitochondrial Dynamics.Molecular neurobiology · 2025Article
- Pediatric acute kidney injury is associated with impairment in nicotinamide adenine dinucleotide (NAD+) metabolism.Pediatric nephrology (Berlin, Germany) · 2025Observational
- Quinoline Quest: Kynurenic Acid Strategies for Next-Generation Therapeutics via Rational Drug Design.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Diverse Physiological Roles of Kynurenine Pathway Metabolites: Updated Implications for Health and Disease.Metabolites · 2025Review
- Gene Expression and Activity of Selected Antioxidant and DNA Repair Enzymes in the Prefrontal Cortex of Sheep as Affected by Kynurenic Acid.International journal of molecular sciences · 2025Article
- Exploring the Neuroprotective Potential of Polyphenolic Compounds in Mitigating Quinolinic Acid-Induced Neurotoxicity in Alzheimer's Disease.Current Alzheimer research · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Quinolinic acid (QUIN), an endogenous metabolite of the kynurenine pathway, is involved in several neurological disorders, including Huntington's disease, Alzheimer's disease, schizophrenia, HIV associated dementia (HAD) etc. QUIN toxicity involves several mechanisms which trigger various metabolic pathways and transcription factors. The primary mechanism exerted by this excitotoxin in the central nervous system (CNS) has been largely related with the overactivation of N-methyl-D-aspartate receptors and increased cytosolic Ca(2+) concentrations, followed by mitochondrial dysfunction, cytochrome c release, ATP exhaustion, free radical formation and oxidative damage. As a result, this toxic pattern is responsible for selective loss of middle size striatal spiny GABAergic neurons and motor alterations in lesioned animals. This toxin has recently gained attention in biomedical research as, in addition to its proven excitotoxic profile, a considerable amount of evidence suggests that oxidative stress and energetic disturbances are major constituents of its toxic pattern in the CNS. Hence, this profile has changed our perception of how QUIN-related disorders combine different toxic mechanisms resulting in brain damage. This review will focus on the description and integration of recent evidence supporting old and suggesting new mechanisms to explain QUIN toxicity.
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Registered trials
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.