ArticleAmerican journal of Alzheimer's disease and other dementias
The Protective Effect of IDO1 Inhibition in Aβ-Treated Neurons and APP/PS1 Mice.
Article in American journal of Alzheimer's disease and other dementias. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Docking Analysis of Drugs Used in the Treatment of Alzheimer's Disease, Using Cell Membrane Receptors and Enzymes of the Kynurenine Pathway: A Pilot Study.International journal of molecular sciences · 2026Article
- Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.Biomolecules · 2026Review
- Kynurenine Pathway, Nrf2 and NF-κB Cross-Regulation in the CNS: An Overview.Molecular neurobiology · 2026Review
- IDO family: the metabolic crossroads connecting immunity, nerves and tumors.Journal of translational medicine · 2026Review
- IDO1 modulates pain sensitivity and comorbid anxiety in chronic migraine through microglial activation and synaptic pruning.Journal of neuroinflammation · 2025Article
- Kynurenine Pathway Dysregulation in Parkinson's Disease: Insights for Disease Modulation and Therapy.International journal of tryptophan research : IJTR · 2025Review
- Alzheimer's disease-specific transcriptomic and epigenomic changes in the tryptophan catabolic pathway.Alzheimer's research & therapy · 2024Article
- The Kynurenine Pathway, Aryl Hydrocarbon Receptor, and Alzheimer's Disease.Brain sciences · 2024Review
- Review
- Potential Effects of Low-Level Toluene Exposure on the Nervous System of Mothers and Infants.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is an inflammatory associated disease, in which dysregulated kynurenine pathway (KP) plays a key role. Through KP, L-tryptophan is catabolized into neurotoxic and neuroprotective metabolites. The overactivation of indolamine 2,3-dioxygenase1 (IDO1), the first rate-limiting enzyme of KP, and the abnormal accumulation of KP metabolites have been noted in AD, and blocking IDO1 has been suggested as a therapeutic strategy. However, the expression patterns of KP enzymes in AD, and whether these enzymes are related to AD pathogenesis, have not been fully studied. Herein, we examined the expression patterns of inflammatory cytokines, neurotrophic factors and KP enzymes, and the activity of IDO1 and IDO1 effector pathway AhR (aryl hydrocarbon receptor) in AD mice. We studied the effects of IDO1 inhibitors on Aβ-related neuroinflammation in rat primary neurons, mouse hippocampal neuronal cells, and APP/PS1 mice. The results further demonstrated the importance of IDO1-catalyzed KP in neuroinflammation in Alzheimer's 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.