Tryptophan and brain disorders

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

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

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

This study investigates how chronic ACTH treatment induces anhedonia-like behavior in rats by altering peripheral inflammation and central dopamine dynamics, with limited reversal by bupropion.

This study shows that kynurenic acid promotes microglia-mediated synaptic pruning in schizophrenia by reducing neuronal activity and linking genetic risk variants to KYNA production.

This study shows that methylglyoxal impairs neuronal function and induces depression by depleting tryptophan and disrupting its metabolism in the brain and intestine.

The paper finds increased levels of neurotoxic metabolites in mild COVID-19 patients, associated with inflammation and hypertension.

The paper constructs a regulatory network model of 44 immune and neurotransmission mediators to show that inflammation is linked to chronic pain, depression, and opioid addiction through increased NF-kB and inflammatory signaling proteins.

This study shows that localized infusion of C20:0 ceramides into the ventral hippocampus of rats activates microglia and induces reversible anhedonia-like behavior.

This study shows that IFN-γ exposure in human iPSC-derived neurons increases MHCI and C4A expression while decreasing synapsin I protein, suggesting a role in neurodevelopmental disorders.

This study examines the effects of maternal immune activation on neurobehavioral development in rhesus monkey offspring, finding reduced gray matter volume in specific brain regions.

This study uses bidirectional Mendelian randomization to investigate causal relationships between inflammatory markers and depression, finding a causal effect of IL-6 on major depressive disorder.

This study identifies variability factors in maternal immune activation models and shows baseline immune responsiveness predicts offspring outcomes.

This study shows that acute mild inflammation from typhoid vaccination alters neurophysiological processes related to attention, specifically increasing alpha suppression in alerting without affecting behavior.

This study shows that maternal immune activation increases the volume of the diagonal domain in rat brains during early postnatal development, with potential sex differences.

This study shows maternal immune activation causes age-specific changes in cytokine receptor expression in offspring's frontal cortex, with potential implications for neuropsychiatric disorders.

This paper investigates how immune activation and tryptophan catabolite pathway activity contribute to memory impairments and schizophrenia symptom dimensions.

The paper evaluates 42 inflammatory markers in MDD cases and controls, finding strong confounding effects and limited predictive power of individual markers for MDD diagnosis.