ArticleEuropean archives of psychiatry and clinical neuroscience2018
Increased quinolinic acid in peripheral mononuclear cells in Alzheimer's dementia.
Article in European archives of psychiatry and clinical neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
- Molecular mechanisms and therapeutic potential of tryptophan metabolism in gut-brain signaling transduction: a narrative review.Journal of neuroinflammation · 2026Review
- Exploring the Neuroprotective Potential of Polyphenolic Compounds in Mitigating Quinolinic Acid-Induced Neurotoxicity in Alzheimer's Disease.Current Alzheimer research · 2025Article
- Tryptophan Metabolism in Alzheimer's Disease with the Involvement of Microglia and Astrocyte Crosstalk and Gut-Brain Axis.Aging and disease · 2024Review
- Role of Kynurenine and Its Derivatives in the Neuroimmune System.International journal of molecular sciences · 2024Review
- Gut Metabolites Acting on the Gut-Brain Axis: Regulating the Functional State of Microglia.Aging and disease · 2024Review
- Rat models of postintracerebral hemorrhage pneumonia induced by nasal inoculation withFrontiers in immunology · 2024Article
- Variations in Quinolinic Acid Levels in Tuberculosis Patients with Diabetes Comorbidity: A Pilot Prospective Cohort Study.Infection and drug resistance · 2024Article
- Quinolinic acid impairs mitophagy promoting microglia senescence and poor healthspan in C. elegans: a mechanism of impaired aging process.Biology direct · 2023Article
- Butyrate ameliorates quinolinic acid-induced cognitive decline in obesity models.The Journal of clinical investigation · 2023Article
- The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases.Biomolecules · 2022Review
- The Kynurenine Pathway-New Linkage between Innate and Adaptive Immunity in Autoimmune Endocrinopathies.International journal of molecular sciences · 2021Review
- Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes.Antioxidants & redox signaling · 2019Review
- Biomarkers for Alzheimer's disease: from pathogenesis to drug development.European archives of psychiatry and clinical neuroscience · 2018Article
- Antidiabetic Drug Metformin Protects Neuronal Cells against Quinolinic Acid-Induced Excitotoxicity by Decreasing Intracellular Calcium.Chonnam medical journal · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of monocytes and macrophages in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD) is poorly understood. Recently, we have shown that the number of CD14+ monocytes remained constant during healthy aging and in AD patients. Although only little is known about the function of activated macrophages and microglia in AD, one important mechanism involves the expression of quinolinic acid (QUIN), an endogenous N-methyl-D-aspartate glutamate receptor (NMDA-R) agonist which mediates excitotoxicity especially in the hippocampus. We used immunofluorescence stainings of PBMCs to determine the expression of quinolinic acid (QUIN) and the MHC class II molecule HLA-DR in peripheral monocytic cells in 51 healthy volunteers aged 22-87 years and 43 patients with AD at diagnosis (0 weeks) and during the course of rivastigmine treatment at 0.25 year (12 weeks), 0.5 year (30 weeks), 1 year, and 1.5 years. The number of QUIN+ HLA-DR+ cells rises in healthy persons aged 30-40 years compared to persons aged 60-70 years, indicating that this cell population increases with aging. AD patients at diagnosis had an increased frequency of QUIN+, QUIN+ HLA-DR+, and QUIN+ HLA-DR+/HLA-DR+ cells compared to aged-matched controls. These cell populations remained increased in AD for up to one year after initiation of treatment with rivastigmine; no alterations were detected in aged healthy persons. We conclude that the expression of the neurotoxic agent QUIN is increased in peripheral monocytes from AD patients. These cells could enter the brain and contribute to excitotoxicity.
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