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Apsara Kandanearatchi et al.
The FEBS journal, 279(8), 1366-1374 (2012-01-21)
This brief review will first consider HIV associated neurocognitive disorder followed by the current understanding of its neuropathogenesis. Against this background the role of the kynurenine pathway will be detailed. Evidence both direct and indirect will be discussed for involvement
Miki Terakata et al.
The Journal of nutrition, 143(7), 1046-1051 (2013-05-24)
In mammals, nicotinamide (Nam) is biosynthesized from l-tryptophan (l-Trp). The enzymes involved in the initial step of the l-Trp→Nam pathway are l-Trp-2,3-dioxygenase (TDO) and indoleamine-2,3-dioxygenase (IDO). We aimed to determine whether tdo-knockout (tdo(-/-)) mice fed a diet without preformed niacin
Alessia Delli Carri et al.
Development (Cambridge, England), 140(2), 301-312 (2012-12-20)
Medium-sized spiny neurons (MSNs) are the only neostriatum projection neurons, and their degeneration underlies some of the clinical features of Huntington's disease. Using knowledge of human developmental biology and exposure to key neurodevelopmental molecules, human pluripotent stem (hPS) cells were
Rafael Lugo-Huitrón et al.
Oxidative medicine and cellular longevity, 2013, 104024-104024 (2013-10-04)
Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in human brain and cerebrospinal fluid (CSF) and is often implicated in the pathogenesis of a variety of human neurological diseases. QUIN is an
Katsumi Shibata et al.
Bioscience, biotechnology, and biochemistry, 77(2), 295-300 (2013-02-09)
Valproic acid (VPA) is a short-chained, branched fatty acid that is widely used in humans as an anticonvulsant and mood stabilizer, and has been reported to increase the liver NAD concentration. We investigated the effects of VPA on the conversion
Age-dependent alterations of the kynurenine pathway in the YAC128 mouse model of Huntington disease.
Gelareh Mazarei et al.
Journal of neurochemistry, 127(6), 852-867 (2013-06-22)
Indoleamine 2,3 dioxygenase (Ido1), the first and rate-limiting enzyme of the kynurenine pathway (KP), is a striatally enriched gene with increased expression levels in the YAC128 mouse model of Huntington disease (HD). Our objective in this study was to delineate
K Saito et al.
Neuroscience, 51(1), 25-39 (1992-11-01)
Accumulation of quinolinic acid and neuroactive kynurenines derived from tryptophan are of potential significance in human neuropathologic diseases because of their neurotoxic and convulsant properties. Clinical studies have established that sustained elevations of quinolinic acid, L-kynurenine and kynurenic acid within
J D Shoemaker et al.
Journal of chromatography, 562(1-2), 125-138 (1991-01-02)
Eighty-five clinical urine samples and nineteen urine samples previously found by other laboratories to suggest genetic metabolic defects were prepared for trimethylsilylation by treatment with urease, followed by azeotropic dehydration. The "Target Analyte Search" program provided with the VG Trio
G Mazarei et al.
Experimental neurology, 249, 144-148 (2013-09-03)
We previously showed that the expression and activity of indoleamine 2,3-dioxygenase (Ido1) are chronically elevated in the striatum of YAC128 mouse model of HD. This was followed by increased production of neurotoxic metabolite hydroxykynurenine (3-HK) in the striatum of symptomatic
Andreas Meinitzer et al.
Clinica chimica acta; international journal of clinical chemistry, 436, 268-272 (2014-06-25)
Quinolinic acid (QA) is thought to be one of the most important metabolites of the kynurenine pathway with the highest biological activity in apoptotic responses and neurodegenerative diseases. The determination of QA might be of clinical relevance in different patient
Sumit Jamwal et al.
Neurotoxicity research, 28(2), 171-184 (2015-06-17)
Huntington disease is hyperkinetic movement disorder characterized by selective and immense degradation of GABAergic medium spiny neurons in striatum. Quinolinic acid (QA)-induced neurotoxicity involves a cascade of events such as excitotoxicity, ATP depletion, oxidative stress, neuroinflammation, as well as selective
Claire Tronel et al.
Oxidative medicine and cellular longevity, 2013, 264935-264935 (2013-03-28)
Heme oxygenase-1 (HO-1) induction is associated with beneficial or deleterious effects depending on the experimental conditions adopted and the neurodegenerative rodent models used. The present study aimed first to evaluate the effects of cerebral HO-1 induction in an in vivo
Julia L Drewes et al.
Journal of neurovirology, 21(4), 449-463 (2015-03-18)
Activation of the kynurenine pathway (KP) of tryptophan catabolism likely contributes to HIV-associated neurological disorders. However, KP activation in brain tissue during HIV infection has been understudied, and the effect of combination antiretroviral therapy (cART) on KP induction in the
G M Megson et al.
Journal of clinical microbiology, 34(1), 218-221 (1996-01-01)
Cryptococcal meningitis (CM) is associated with raised intracranial pressure which is linked with serious neurological sequelae. Cryptococcus neoformans produces D-mannitol in vitro and in experimental meningitis in rabbits. Mannitol present in the cerebrospinal fluid (CSF) of CM patients could exacerbate
Kynurenine pathway enzymes in brain. Properties of enzymes and regulation of quinolinic acid synthesis.
K Saito et al.
Advances in experimental medicine and biology, 398, 485-492 (1996-01-01)
A L Colín-González et al.
Neuroscience, 231, 91-101 (2012-12-04)
Quinolinic acid (QA)-induced overactivation of N-methyl-d-aspartate receptors yields excitotoxicity, oxidative stress and mitochondrial dysfunction, which altogether contribute to trigger a wide variety of toxic pathways with biochemical, behavioral and neuropathological alterations similar to those observed in Huntington's disease. Noteworthy, in
A S Basile et al.
Gastroenterology, 108(3), 818-823 (1995-03-01)
Quinolinic acid is an endogenous neuroexcitant derived from tryptophan. Brain quinolinic acid concentrations are reportedly elevated in chronic liver failure. The aim of this study was to determine if brain quinolinic acid levels correlate with the severity of hepatic encephalopathy.
D W Ellison et al.
Brain : a journal of neurology, 110 ( Pt 6), 1657-1673 (1987-12-01)
Concentrations of gamma-aminobutyric acid (GABA), glutamate, aspartate, and taurine were measured in postmortem tissue from the brains of patients with Huntington's disease (HD) and in the quinolinic acid (QA) lesioned rat striatum. The aim of the study was to assess
F Guneral et al.
Clinical chemistry, 40(6), 862-866 (1994-06-01)
Organic acid concentrations were quantified by gas chromatography and the individual acids identified by mass spectrometry in urine specimens from a healthy Turkish pediatric population of ages 2 days to 16 years, subdivided into five age groups. We quantified 69
M Ellaurie et al.
The Pediatric infectious disease journal, 11(4), 286-289 (1992-04-01)
Neopterin concentrations in 50 children with human immunodeficiency virus infection were correlated with disease course. The neopterin concentrations ranged from 4 to 70 nM with a mean of 34.7 +/- 25.1 (SD) nM compared with a mean of 6.1 +/-
Gilles J Guillemin et al.
Neurotoxicity research, 7(1-2), 103-123 (2005-01-11)
Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous
Koenraad F van der Sluijs et al.
Thorax, 68(12), 1122-1130 (2013-07-25)
Patients with allergic asthma have exacerbations which are frequently caused by rhinovirus infection. The antiviral tryptophan-catabolising enzyme indoleamine 2,3-dioxygenase (IDO) is induced by interferon-γ and suppressed by Th2 mediators interleukin (IL)-4 and IL-13. We hypothesised that local IDO activity after
C Power et al.
The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques, 22(2), 92-100 (1995-05-01)
HIV-1 infection is characterized by multiple neurological syndromes occurring at all stages of infection. HIV-1-associated dementia, however, is the most devastating CNS consequence of AIDS because of its poor prognosis and functional impairment. A clinical triad of progressive cognitive decline
L E Horsfall et al.
Antimicrobial agents and chemotherapy, 51(6), 2136-2142 (2007-02-20)
Various inhibitors of metallo-beta-lactamases have been reported; however, none are effective for all subgroups. Those that have been found to inhibit the enzymes of subclass B2 (catalytically active with one zinc) either contain a thiol (and show less inhibition towards
Nathan R Rose et al.
Journal of medicinal chemistry, 51(22), 7053-7056 (2008-10-24)
The dynamic methylation of histone lysyl residues plays an important role in biology by regulating transcription, maintaining genomic integrity, and by contributing to epigenetic effects. Here we describe a variety of inhibitor scaffolds that inhibit the human 2-oxoglutarate-dependent JMJD2 subfamily
Phedias Diamandis et al.
Nature chemical biology, 3(5), 268-273 (2007-04-10)
The identification of self-renewing and multipotent neural stem cells (NSCs) in the mammalian brain holds promise for the treatment of neurological diseases and has yielded new insight into brain cancer. However, the complete repertoire of signaling pathways that governs the
Paula Pierozan et al.
Brain research, 1577, 1-10 (2014-07-01)
Quinolinic acid (QUIN) is a neuroactive metabolite of the kinurenine pathway, considered to be involved in aging and some neurodegenerative disorders, including Huntington׳s disease. In the present work we have studied the long-lasting effect of acute intrastriatal injection of QUIN
Paula Pierozan et al.
The FEBS journal, 281(8), 2061-2073 (2014-03-13)
Quinolinic acid (QUIN) is a neuroactive metabolite of the kinurenine pathway, and is considered to be involved in aging and some neurodegenerative disorders, including Huntington's disease. QUIN was injected intrastriatally into adolescent rats, and biochemical and histopathological analyses in the
Yukio Seki et al.
Neurochemical research, 30(1), 123-128 (2005-03-11)
In the experimental setting, taurine is known to be released from swollen cells to reestablish their normal volume. However, its clinical relevance has not been fully understood. This study was undertaken to reveal changes in cerebrospinal fluid (CSF) amino acids
Isabelle M Medana et al.
The Journal of infectious diseases, 188(6), 844-849 (2003-09-10)
A retrospective study of 100 Malawian children (87 with malaria and 13 with a diagnosis other than malaria) was conducted to determine the relationship between levels of metabolites of the kynurenine pathway in cerebrospinal fluid (CSF) and disease outcome. Three
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