ReviewProgress in neurobiology2010
Of mice, rats and men: Revisiting the quinolinic acid hypothesis of Huntington's disease.
Review in Progress in neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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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.
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Who cites it
75 citing papers in PubMed, 173 citations in OpenAlex.
- Early hypoxia-induced secretome remodeling reveals adaptive mechanisms and biomarkers of blood-brain barrier dysfunction in ischemic stroke.Molecular brain · 2026Article
- Avocado Oil Prevents Neurological and Behavioral Alterations in a Quinolinic Acid-Induced Model of Huntington's Disease.Neurochemical research · 2025Article
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- NMDA Receptors: Distribution, Role, and Insights into Neuropsychiatric Disorders.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The Complex World of Kynurenic Acid: Reflections on Biological Issues and Therapeutic Strategy.International journal of molecular sciences · 2024Review
- Probiotics relieve perioperative postoperative cognitive dysfunction induced by cardiopulmonary bypass through the kynurenine metabolic pathway.Scientific reports · 2024Article
- A pilot investigation of the association between HIV-1 Vpr amino acid sequence diversity and the tryptophan-kynurenine pathway as a potential mechanism for neurocognitive impairment.Virology journal · 2024Article
- From Pathogenesis to Therapeutics: A Review of 150 Years of Huntington's Disease Research.International journal of molecular sciences · 2023Review
- Pharmacological Characterization of [Molecular imaging and biology · 2023Article
- Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies.Aging and disease · 2023Review
- Toll-Like Receptor 4 Plays a Significant Role in the Biochemical and Neurological Alterations Observed in Two Distinct Mice Models of Huntington's Disease.Molecular neurobiology · 2023Article
- Exploring the neuroprotective effects of montelukast on brain inflammation and metabolism in a rat model of quinolinic acid-induced striatal neurotoxicity.Journal of neuroinflammation · 2023Article
- Quinolinic Acid Induces Alterations in Neuronal Subcellular Compartments, Blocks Autophagy Flux and Activates Necroptosis and Apoptosis in Rat Striatum.Molecular neurobiology · 2022Article
- Migraine signaling pathways: amino acid metabolites that regulate migraine and predispose migraineurs to headache.Molecular and cellular biochemistry · 2022Review
- An integrated cytokine and kynurenine network as the basis of neuroimmune communication.Frontiers in neuroscience · 2022Review
- Research Models of the Nanoparticle-Mediated Drug Delivery across the Blood-Brain Barrier.Tissue engineering and regenerative medicine · 2021Review
- Caenorhabditis elegans as a model for studies on quinolinic acid-induced NMDAR-dependent glutamatergic disorders.Brain research bulletin · 2021Article
- Alterations of kynurenine pathway in alcohol use disorder and abstinence: a link with gut microbiota, peripheral inflammation and psychological symptoms.Translational psychiatry · 2021Article
- New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021Review
- Huntington's Chorea-a Rare Neurodegenerative Autosomal Dominant Disease: Insight into Molecular Genetics, Prognosis and Diagnosis.Applied biochemistry and biotechnology · 2021Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The neurodegenerative disease Huntington's disease (HD) is caused by an expanded polyglutamine (polyQ) tract in the protein huntingtin (htt). Although the gene encoding htt was identified and cloned more than 15 years ago, and in spite of impressive efforts to unravel the mechanism(s) by which mutant htt induces nerve cell death, these studies have so far not led to a good understanding of pathophysiology or an effective therapy. Set against a historical background, we review data supporting the idea that metabolites of the kynurenine pathway (KP) of tryptophan degradation provide a critical link between mutant htt and the pathophysiology of HD. New studies in HD brain and genetic model organisms suggest that the disease may in fact be causally related to early abnormalities in KP metabolism, favoring the formation of two neurotoxic metabolites, 3-hydroxykynurenine and quinolinic acid, over the related neuroprotective agent kynurenic acid. These findings not only link the excitotoxic hypothesis of HD pathology to an impairment of the KP but also define new drug targets and therefore have direct therapeutic implications. Thus, pharmacological normalization of the imbalance in brain KP metabolism may provide clinical benefits, which could be especially effective in early stages of the disease.
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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.