Journal ArticleDOI
Tryptophan metabolism and brain function: focus on kynurenine and other indole metabolites
TLDR
A number of metabolites affecting brain function originate from tryptophan metabolism and selective inhibitors of their forming enzymes may be useful to understand their role in physiology or as therapeutic agents in pathology.About:
This article is published in European Journal of Pharmacology.The article was published on 1999-06-30. It has received 337 citations till now. The article focuses on the topics: Kynurenine pathway & Kynurenine.read more
Citations
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NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences
TL;DR: Future investigation into the metabolism and biological functions of NAD and NADP may expose fundamental properties of life, and suggest new strategies for treating diseases and slowing the aging process.
Journal ArticleDOI
Kynurenines in the mammalian brain: when physiology meets pathology
TL;DR: With recently developed pharmacological agents, it is now possible to restore metabolic equilibrium and envisage novel therapeutic interventions on the basis of the kynurenine pathway.
Journal ArticleDOI
The Brain Metabolite Kynurenic Acid Inhibits α7 Nicotinic Receptor Activity and Increases Non-α7 Nicotinic Receptor Expression: Physiopathological Implications
Corey Hilmas,Edna F. R. Pereira,Manickavasagom Alkondon,Arash Rassoulpour,Robert Schwarcz,Edson X. Albuquerque +5 more
TL;DR: It is demonstrated that nAChRs are targets for KYNA and suggest a functionally significant cross talk between the nicotinic cholinergic system and the kynurenine pathway in the brain.
Journal ArticleDOI
Gene microarrays in hippocampal aging: statistical profiling identifies novel processes correlated with cognitive impairment.
Eric M. Blalock,Kuey-Chu Chen,Keith M Sharrow,James P. Herman,Nada M. Porter,Thomas C. Foster,Philip W. Landfield +6 more
TL;DR: A new integrative model of brain aging is suggested in which genomic alterations in early adulthood initiate interacting cascades of decreased signaling and synaptic plasticity in neurons, extracellular changes, and increased myelin turnover-fueled inflammation in glia that cumulatively induce aging-related cognitive impairment.
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Increased cortical kynurenate content in schizophrenia.
Robert Schwarcz,Arash Rassoulpour,Hui Qiu Wu,Deborah R. Medoff,Carol A. Tamminga,Rosalinda C. Roberts +5 more
TL;DR: In rats, chronic treatment with haloperidol did not cause an increase in kynurenate levels in the frontal cortex, indicating that the elevation observed in schizophrenia is not due to antipsychotic medication.
References
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Prevention of allogeneic fetal rejection by tryptophan catabolism
David H. Munn,Min Zhou,John T. Attwood,Igor Bondarev,Simon J. Conway,Brendan Marshall,Corrie C. Brown,Andrew L. Mellor +7 more
TL;DR: In 1953 Medawar pointed out that survival of the genetically disparate (allogeneic) mammalian conceptus contradicts the laws of tissue transplantation and suppresses T cell activity and defends itself against rejection.
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Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain.
TL;DR: In rats ischemia of the forebrain induced by a 30-minute occlusion of the carotid artery, followed by 120 minutes of arterial reperfusion, produced ischemic lesions of selectively vulnerable pyramidal cells in both hippocampi.
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Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
TL;DR: It is demonstrated that lesions due to quinolinic acid closely resemble those of HD as they result in marked depletions of both GABA and substance P, with selective sparing of somatostatin/neuropeptide Y neurones.
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Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain
TL;DR: Intracerebral injection of the neuroexcitatory tryptophan metabolite, quinolinic acid, has behavioral, neurochemical and neuropathological consequences reminiscent of those of exogenous excitotoxins, such as kainic and ibotenic acids.