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Kynurenine Pathway Metabolites in Humans: Disease and Healthy States
Yiquan Chen and Gilles J. Guillemin
International Journal of Tryptophan Research , 2012,
Abstract: Tryptophan is an essential amino acid that can be metabolised through different pathways, a major route being the kynurenine pathway. The first enzyme of the pathway, indoleamine-2,3-dioxygenase, is strongly stimulated by inflammatory molecules, particularly interferon gamma. Thus, the kynurenine pathway is often systematically up-regulated when the immune response is activated. The biological significance is that 1) the depletion of tryptophan and generation of kynurenines play a key modulatory role in the immune response; and 2) some of the kynurenines, such as quinolinic acid, 3-hydroxykynurenine and kynurenic acid, are neuroactive. The kynurenine pathway has been demonstrated to be involved in many diseases and disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, AIDS dementia complex, malaria, cancer, depression and schizophrenia, where imbalances in tryptophan and kynurenines have been found. This review compiles most of these studies and provides an overview of how the kynurenine pathway might be contributing to disease development, and the concentrations of tryptophan and kynurenines in the serum, cerebrospinal fluid and brain tissues in control and patient subjects.
Kynurenine Pathway Metabolites in Humans: Disease and Healthy States
Yiquan Chen,Gilles J. Guillemin
International Journal of Tryptophan Research , 2009,
Abstract: Tryptophan is an essential amino acid that can be metabolised through different pathways, a major route being the kynurenine pathway. The first enzyme of the pathway, indoleamine-2,3-dioxygenase, is strongly stimulated by inflammatory molecules, particularly interferon gamma. Thus, the kynurenine pathway is often systematically up-regulated when the immune response is activated. The biological significance is that 1) the depletion of tryptophan and generation of kynurenines play a key modulatory role in the immune response; and 2) some of the kynurenines, such as quinolinic acid, 3-hydroxykynurenine and kynurenic acid, are neuroactive. The kynurenine pathway has been demonstrated to be involved in many diseases and disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, AIDS dementia complex, malaria, cancer, depression and schizophrenia, where imbalances in tryptophan and kynurenines have been found. This review compiles most of these studies and provides an overview of how the kynurenine pathway might be contributing to disease development, and the concentrations of tryptophan and kynurenines in the serum, cerebrospinal fluid and brain tissues in control and patient subjects.
Glycogen Synthase Kinase-3 is an Intermediate Modulator of Serotonin Neurotransmission  [PDF]
Abigail M. Polter,Xiaohua Li
Frontiers in Molecular Neuroscience , 2011, DOI: 10.3389/fnmol.2011.00031
Abstract: Serotonin is a neurotransmitter with broad functions in brain development, neuronal activity, and behaviors; and serotonin is the prominent drug target in several major neuropsychiatric diseases. The multiple actions of serotonin are mediated by diverse serotonin receptor subtypes and associated signaling pathways. However, the key signaling components that mediate specific function of serotonin neurotransmission have not been fully identified. This review will provide evidence from biochemical, pharmacological, and animal behavioral studies showing that serotonin regulates the activation states of brain glycogen synthase kinase-3 (GSK3) via type 1 and type 2 serotonin receptors. In return, GSK3 directly interacts with serotonin receptors in a highly selective manner, with a prominent effect on modulating serotonin 1B receptor activity. Therefore, GSK3 acts as an intermediate modulator in the serotonin neurotransmission system, and balanced GSK3 activity is essential for serotonin-regulated brain function and behaviors. Particularly important, several classes of serotonin-modulating drugs, such as antidepressants and atypical antipsychotics, regulate GSK3 by inhibiting its activity in brain, which reinforces the importance of GSK3 as a potential therapeutic target in neuropsychiatric diseases associated with abnormal serotonin function.
Book Review-"Pathways to the Common Core"  [cached]
Sharilyn C. Steadman
Journal of Curriculum and Instruction , 2013,
Abstract: Book review of "Pathways to the Common Core: Accelerating Achievement" by L. Caulkins, M. Ehrenworth, and C. Lehman.
Serotonin Syndrome
Harold Mu?oz Cortés,Adriana Vargas Rueda
MedUNAB , 2004,
Abstract: The serotonin syndrome is a clinical condition associated with serotonin agonists, prescribed to treat some psychiatric and non psychiatric diseases like affective, anxiety and pain disorders. Is due to an excessive stimulation of central and peripheral serotonin receptors that leads to mental, autonomic and neuromuscular changes. Usually the disorder resolves within the first 24 hours after the medications are discontinued, however some patients progress to a multiple organ failure and die. This paper is a theoretical review of the fundamental aspects of the serotonin syndrome, beginning with a brief review of the anatomic and physiologic features of serotonin system, to continue to examine the most relevant historic, diagnosis, clinical and treatment aspects of the syndrome.
Serotonin and circadian rhythms
Pontes, André Luiz Bezerra de;Engelberth, Rovena Clara Galv?o Januário;Nascimento, Jr., Expedito da Silva;Cavalcante, Judney Cley;Costa, Miriam Stela Maris de Oliveira;Pinato, Luciana;Toledo, Claudio Antonio Barbosa de;Cavalcante, Jeferson de Souza;
Psychology & Neuroscience , 2010, DOI: 10.3922/j.psns.2010.2.011
Abstract: all mammal behaviors and functions exhibit synchronization with environmental rhythms. this is accomplished through an internal mechanism that generates and modulates biological rhythms. the circadian timing system, responsible for this process, is formed by connected neural structures. pathways receive and transmit environmental cues to the central oscillator, the hypothalamic suprachiasmatic nucleus, which mediates physiological and behavioral alterations. the suprachiasmatic nucleus has three major inputs: the retinohypothalamic tract (a direct projection from the retina), the geniculohypothalamic tract (an indirect photic projection originating in the intergeniculate leaflet), and a dense serotonergic plexus from the raphe nuclei. the serotonergic pathway, a source of non-photic cues to the suprachiasmatic nucleus, modulates its activity. the importance of raphe nuclei in circadian rhythms, especially in photic responses, has been demonstrated in many studies. serotonin is the raphe neurotransmitter that triggers phase shifts, inhibits light-induced phase-shifts, and plays a role in controlling the sleep-wake cycle. all data to date have demonstrated the importance of the raphe, through serotonergic afferents, in adjusting circadian rhythms and must therefore be considered a component of the circadian timing system. the aim of this paper is to review the literature addressing the involvement of serotonin in the modulation of circadian rhythm.
Serotonin and circadian rhythms
André Luiz Bezerra de Pontes,Rovena Clara Galv?o Januário Engelberth,Expedito da Silva Nascimento Jr.,Judney Cley Cavalcante
Psychology & Neuroscience , 2010,
Abstract: All mammal behaviors and functions exhibit synchronization with environmental rhythms. This is accomplished through an internal mechanism that generates and modulates biological rhythms. The circadian timing system, responsible for this process, is formed by connected neural structures. Pathways receive and transmit environmental cues to the central oscillator, the hypothalamic suprachiasmatic nucleus, which mediates physiological and behavioral alterations. The suprachiasmatic nucleus has three major inputs: the retinohypothalamic tract (a direct projection from the retina), the geniculohypothalamic tract (an indirect photic projection originating in the intergeniculate leaflet), and a dense serotonergic plexus from the raphe nuclei. The serotonergic pathway, a source of non-photic cues to the suprachiasmatic nucleus, modulates its activity. The importance of raphe nuclei in circadian rhythms, especially in photic responses, has been demonstrated in many studies. Serotonin is the raphe neurotransmitter that triggers phase shifts, inhibits light-induced phase-shifts, and plays a role in controlling the sleep-wake cycle. All data to date have demonstrated the importance of the raphe, through serotonergic afferents, in adjusting circadian rhythms and must therefore be considered a component of the circadian timing system. The aim of this paper is to review the literature addressing the involvement of serotonin in the modulation of circadian rhythm.
Transient Serotonin Syndrome by Concurrent Use of Electroconvulsive Therapy and Selective Serotonin Reuptake Inhibitor: A Case Report and Review of the Literature
Nagahisa Okamoto,Kota Sakamoto,Maki Yamada
Case Reports in Psychiatry , 2012, DOI: 10.1155/2012/215214
Abstract: The serotonin syndrome, which is characterized by psychiatric, autonomic nervous and neurological symptoms, is considered to be caused by excessive stimulation of the 5-HT1A and 5-HT2 receptors in the gray matter and spinal cord of the central nervous system, after the start of dosing or increase of the dose of a serotoninergic drug. There have been hardly any reports of induction of serotonin syndrome by electroconvulsive therapy (ECT) in combination with antidepressant. We present the case of a female patient with major depressive disorder (MDD) who developed transient serotonin syndrome soon after the first session of ECT in combination with paroxetine. Paroxetine was discontinued, and her psychiatric, autonomic nervous and neurological symptoms were gradually relieved and disappeared within 2 days. We performed the second ECT session 5 days after the initial session and performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of SS were observed. Finally, her MDD remitted. ECT might cause transiently increased blood-brain barrier (BBB) permeability and enhance the transmissivity of the antidepressant in BBB. Therefore, it is necessary to pay attention to rare side effect of serotonin syndrome by ECT in combination with antidepressant.
Tryptophan-Kynurenine Metabolism and Insulin Resistance in Hepatitis C Patients  [PDF]
G. F. Oxenkrug,W. A. Turski,W. Zgrajka,J. V. Weinstock,P. Summergrad
Hepatitis Research and Treatment , 2013, DOI: 10.1155/2013/149247
Abstract: Chronic hepatitis C virus (HCV) infection is associated with 50% incidence of insulin resistance (IR) that is fourfold higher than that in non-HCV population. IR impairs the outcome of antiviral treatment. The molecular mechanisms of IR in HCV are not entirely clear. Experimental and clinical data suggested that hepatitis C virus per se is diabetogenic. However, presence of HCV alone does not affect IR. It was proposed that IR is mediated by proinflammatory cytokines, mainly by TNF-alpha. TNF-alpha potentiates interferon-gamma-induced transcriptional activation of indoleamine 2,3-dioxygenase, the rate-limiting enzyme of tryptophan- (TRP-) kynurenine (KYN) metabolism. Upregulation of TRP-KYN metabolism was reported in HCV patients. KYN and some of its derivatives affect insulin signaling pathways. We hypothesized that upregulation of TRP-KYN metabolism might contribute to the development of IR in HCV. To check this suggestion, we evaluated serum concentrations of TRP and KYN and HOMA-IR and HOMA-beta in 60 chronic HCV patients considered for the treatment with IFN-alpha. KYN and TRP concentrations correlated with HOMA-IR and HOMA-beta scores. Our data suggest the involvement of KYN and its metabolites in the development of IR in HCV patients. TRP-KYN metabolism might be a new target for prevention and treatment of IR in HCV patients. 1. Introduction Hepatitis C patients have fourfold higher incidence of insulin resistance (IR) than non-HCV population, that is, healthy controls or chronic hepatitis B patients [1]. IR is the major feature of the metabolic syndrome (diabetes type 2, obesity, hypertension, and cardiovascular disorders). HCV-associated IR may lead to resistance to antiviral therapy, hepatocarcinogenesis, and extrahepatic complications [2, 3]. The molecular mechanisms whereby HCV infection leads to IR are not entirely clear. Experimental and clinical findings indicated that hepatitis C virus per se is diabetogenic [4, 5]. However, presence of HCV alone does not affect IR [6]. It was suggested that increased production of proinflammatory cytokines, especially TNF-alpha, contributes to the development of IR in HCV patients [7]. TNF-alpha potentiates interferon-gamma- (IFNG-) triggered transcriptional induction of indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme of tryptophan- (TRP-) kynurenine (KYN) metabolism [8]. Upregulated IDO expression in the dendritic cells [9] and in the liver [10] and increased serum KYN?:?TRP ratio (KTR) [10] were reported for HCV patients. Review of clinical and experimental data suggested that KYN and some
Transient Serotonin Syndrome by Concurrent Use of Electroconvulsive Therapy and Selective Serotonin Reuptake Inhibitor: A Case Report and Review of the Literature  [PDF]
Nagahisa Okamoto,Kota Sakamoto,Maki Yamada
Case Reports in Psychiatry , 2012, DOI: 10.1155/2012/215214
Abstract: The serotonin syndrome, which is characterized by psychiatric, autonomic nervous and neurological symptoms, is considered to be caused by excessive stimulation of the 5-HT1A and 5-HT2 receptors in the gray matter and spinal cord of the central nervous system, after the start of dosing or increase of the dose of a serotoninergic drug. There have been hardly any reports of induction of serotonin syndrome by electroconvulsive therapy (ECT) in combination with antidepressant. We present the case of a female patient with major depressive disorder (MDD) who developed transient serotonin syndrome soon after the first session of ECT in combination with paroxetine. Paroxetine was discontinued, and her psychiatric, autonomic nervous and neurological symptoms were gradually relieved and disappeared within 2 days. We performed the second ECT session 5 days after the initial session and performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of SS were observed. Finally, her MDD remitted. ECT might cause transiently increased blood-brain barrier (BBB) permeability and enhance the transmissivity of the antidepressant in BBB. Therefore, it is necessary to pay attention to rare side effect of serotonin syndrome by ECT in combination with antidepressant. 1. Introduction The serotonin syndrome, which is characterized by psychiatric, autonomic nervous and neurological symptoms, is considered to be caused by excessive stimulation of the 5-HT1A and 5-HT2 receptors in the gray matter and spinal cord of the central nervous system after the start of dosing or increase of the dose of a serotoninergic drug [1]. There have been hardly any reports of induction of serotonin syndrome by electroconvulsive therapy (ECT) in combination with antidepressant. We present the case of a female patient with major depressive disorder (MDD) who developed transient serotonin syndrome soon after the first session of ECT in combination with paroxetine. 2. Case Presentation Mrs. T was a 67-year-old woman who had no past history of physical disease and had no psychiatric family history. In June 2008, she experienced depressed mood, decreased energy, anxiety, agitation, and insomnia, and she visited a psychiatric clinic. She was diagnosed with MDD. She took milnacipran (30?mg/day), but her depressive symptoms became more serious gradually without a change of the medication around December 2008. She completely lost interest in her leisure activity. In April 2009, she developed physical symptoms such as a respiratory discomfort. She was examined in many
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