Tryptophan and brain disorders

This study identifies IFNγ-driven immune-metabolic changes in lupus-prone mice that lead to serotonin-kynurenine imbalance and cortical vulnerability.

This paper develops IFN-β as a safe in-vivo model of human inflammation, inducing robust sickness responses with minimal cardiovascular effects in healthy volunteers aged 18-75.

This study identifies novel biomarkers in atypical depression with psychotic symptoms using multi-omics and brain organoids, revealing immune and neurological alterations.

The paper shows that Kmo produces 3-HK, which promotes macrophage lysosomal acidification via kainate receptor antagonism, enhancing resistance to Salmonella infection.

This study identifies how peripheral inflammation reduces serotonin neuron signaling through IL-1R1-mediated pathways, decreasing neuronal excitability and increasing serotonin clearance.

This study maps tryptophan metabolites across multiple tissues, sexes, and ages in mice, revealing significant variations in metabolism that could inform disease-targeted therapies.

The paper identifies MRI-derived markers in the VTA linked to depression diagnosis and symptom severity, showing distinct patterns of neuroinflammation and microstructural changes.

This study shows that systemic inflammation increases exploitative behavior in mice during patch-foraging tasks, suggesting a link between immunometabolic states and decision-making.

This study compares serum tryptophan pathway alterations in chronic METH and MDMA users, finding distinct metabolic changes linked to psychiatric symptoms.

The paper identifies a monocyte dysregulation signature in MDD linked to clinical symptoms using CITE-Seq data from PBMCs.

This study shows that Lcn2 deficiency causes social impairments in offspring independent of maternal immune activation, with no additive effects when combined.

This study identifies two clusters of severe mental disorder patients with differing illness severity, finding elevated pro-inflammatory serum proteins in the more severe group.

This study shows that BT2, an inhibitor of BCKDK, reduces plasma tryptophan by displacing it from albumin, revealing an off-target effect on tryptophan metabolism.

The paper develops a computational model to explore how inflammation, serotonin levels, and brain activity interact, and how anti-inflammatory and antidepressant treatments affect depressive symptoms.

This study shows that parental Kmo genotype affects offspring behavior and sleep in sex-specific ways through changes in the kynurenine pathway and brain mitochondrial function.

The paper shows N-formylkynurenine (NFK) undergoes non-enzymatic deamination to form reactive adducts, distinct from kynurenine (KYN), highlighting a new branch of the kynurenine pathway with implications for immune regulation and protein modification.

This study examines how changes in kynurenine pathway metabolite ratios relate to antidepressant response in patients treated with SSRIs, finding specific shifts in neuroprotective-to-neurotoxic metabolite balances.

This study shows that overactivation of prefrontal astrocytes in mice impairs cognition and PV interneuron function through increased kynurenine pathway metabolite KYNA.

This study uses GRIT to measure tryptophan dynamics across species and scales, revealing links between tryptophan metabolism, inflammation, and behavior.

The paper identifies synaptic-related gene dysregulation in PBMCs of MDD patients, highlighting shared molecular signatures with brain regions and potential biomarkers for depression.

This study establishes a novel mouse model of prenatal IL-17A imprinting, showing embryo-restricted responses lead to behavioral deficits in offspring.

The paper identifies intron retention (IR) as a biomarker for depression and shows its utility in discovering recovery pathways through RNA-seq analysis of peripheral blood mononuclear cells.

The paper shows that reduced IKZF1 and IKZF2 in immune cells of schizophrenic patients leads to impaired neural circuits and schizophrenia-like symptoms in mice and human cell models.

The paper investigates the combined effects of maternal immune activation and adolescent THC exposure in rats, revealing brain and transcriptomic changes without overt behavioral disruptions.

This study identifies thalamostriatal circuit disruption as a conserved neuroinflammatory mechanism linking systemic inflammation to depression and anhedonia in humans and mice.

This study shows that kynurenic acid (KYNA) and its enzyme KAT II expand in primate dlPFC, impairing cognitive functions by affecting NMDA and nic-7Rs, and suggests targeting KYNA as a therapeutic approach for neuroinflammatory disorders.

This study identifies quinolinic acid as a key metabolite linking kidney injury to brain toxicity through the kynurenine pathway in mice and humans.

This study shows that LPS-induced inflammation reduces GABAergic interneuron markers and BDNF in mouse prefrontal cortex and hippocampus, suggesting a link to MDD pathophysiology.

This study uses metabolomics to analyze changes in mouse embryonic CSF after maternal immune activation, identifying elevated glucocorticoids and kynurenine pathway metabolites.