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Article ; Online: Cortical kynurenine pathway metabolism: a novel target for cognitive enhancement in Schizophrenia.

Wonodi, Ikwunga / Schwarcz, Robert

2010 Volume 36, Issue 2, Page(s) 211–218

Abstract: The brain concentration of kynurenic acid (KYNA), a metabolite of the kynurenine pathway of tryptophan degradation and antagonist at both the glycine coagonist site of the N-methyl-D-aspartic acid receptor (NMDAR) and the alpha7 nicotinic acetylcholine ... ...

Abstract	The brain concentration of kynurenic acid (KYNA), a metabolite of the kynurenine pathway of tryptophan degradation and antagonist at both the glycine coagonist site of the N-methyl-D-aspartic acid receptor (NMDAR) and the alpha7 nicotinic acetylcholine receptor (alpha7nAChR), is elevated in the prefrontal cortex (PFC) of individuals with schizophrenia. This increase may be clinically relevant because hypofunction of both the NMDAR and the alpha7nAChR are implicated in the pathophysiology, and especially in the cognitive deficits associated with the disease. In rat PFC, fluctuations in endogenous KYNA levels bidirectionally modulate extracellular levels of 3 neurotransmitters closely related to cognitive function (glutamate, dopamine, and acetylcholine). Moreover, behavioral studies in rats have demonstrated a causal link between increased cortical KYNA levels and neurocognitive deficits, including impairment in spatial working memory, contextual learning, sensory gating, and prepulse inhibition of the startle reflex. In recent human postmortem studies, impairments in gene expression and activity of kynurenine pathway enzymes were found in cortical areas of individuals with schizophrenia. Additional studies have revealed an interesting association between a sequence variant in the gene of one of these enzymes, kynurenine 3-monooxygenase, and neurocognitive deficits seen in patients. The emerging, remarkable confluence of data from humans and animals suggests an opportunity for developing a rational pharmacology by targeting cortical kynurenine pathway metabolism for cognition enhancement in schizophrenia and beyond.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/physiology ; Cognition Disorders/drug therapy ; Cognition Disorders/physiopathology ; Disease Models, Animal ; Humans ; Kynurenine/metabolism ; Neurotransmitter Agents/metabolism ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/physiopathology ; Rats ; Receptors, Nicotinic/drug effects ; Receptors, Nicotinic/physiology ; Schizophrenia/drug therapy ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; alpha7 Nicotinic Acetylcholine Receptor
Chemical Substances	Chrna7 protein, human ; Chrna7 protein, rat ; Neurotransmitter Agents ; Receptors, Nicotinic ; alpha7 Nicotinic Acetylcholine Receptor ; Kynurenine (343-65-7)
Language	English
Publishing date	2010-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	439173-1
ISSN	1745-1701 ; 0586-7614
ISSN (online)	1745-1701
ISSN	0586-7614
DOI	10.1093/schbul/sbq002
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Article ; Online: Clozapine and neutrophil response in patients of African descent: A six-month, multinational, prospective, open-label clinical trial.

Kelly, Deanna L / Glassman, Matthew / Wonodi, Ikwunga / Vyas, Gopal / Richardson, Charles M / Nwulia, Evaristus / Wehring, Heidi J / Oduguwa, Taiwo / Mackowick, Marie / Hipolito, Maria Mananita S / Peters, Olawunmi / Rai, Narayan / Park, Jaeboon / Adebayo, Adeola O / Gorelick, David A / Weiner, Elaine / Liu, Fang / Kearns, Ann Marie / Adams, Heather A /

Love, Raymond C / Chen, Shuo / Olaniyan, Ayodeji / Ambulos, Nicholas / McKoy, Darius / Nallani, Madhulika C / Lanzkron, Sophie / Mengistab, Mulu / Barr, Brian / Davis, Erica / Lawal, Rahman / Buchanan, Robert W / Adebayo, Richard

Schizophrenia research

2023

Abstract: Introduction: Clozapine is the most effective antipsychotic for treatment-resistant schizophrenia, but it is markedly underutilized, particularly in the US Black population, partly because of concern over clozapine-associated low absolute neutrophil ... ...

Abstract	Introduction: Clozapine is the most effective antipsychotic for treatment-resistant schizophrenia, but it is markedly underutilized, particularly in the US Black population, partly because of concern over clozapine-associated low absolute neutrophil count (ANC). People of African descent have a lower normative ANC range than the White population, which is associated with a specific "ACKR1-null" ("Duffy null") CC genotype (SNP rs2814778) on the ACKR1 gene, termed benign ethnic neutropenia (BEN). The range of ANC variability and safety of clozapine have not been established in people with BEN or examined prospectively in people of African descent. Methods: We completed a multisite, 6-month, prospective, open-label clinical trial of clozapine treatment in people of African descent with schizophrenia spectrum disorders for whom clozapine was clinically indicated, with or without the ACKR1-null genotype. We examined clozapine safety and weekly ANC during clozapine treatment and evaluated ANC variability by ACKR1-null genotype, sex, study site, and clozapine dosing using repeated measures analysis of covariance. Genotype was assayed using TaqMan® technology. Results: We enrolled 274 participants, of whom 227 (82.8 %) completed 6 months of clozapine treatment. There was one case of severe neutropenia (<500 cells/mm Conclusion: To our knowledge, this is the largest prospective clozapine trial in people of African descent. Severe neutropenia was rare, despite the high prevalence (80 %) of the ACKR1-null genotype. Our findings suggest that clozapine can be used safely in Black patients including those with BEN.
Language	English
Publishing date	2023-08-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2023.08.002
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Article ; Online: Clozapine in Reducing Aggression and Violence in Forensic Populations.

Patchan, Kathleen / Vyas, Gopal / Hackman, Ann L / Mackowick, Marie / Richardson, Charles M / Love, Raymond C / Wonodi, Ikwunga / Sayer, MacKenzie A / Glassman, Matthew / Feldman, Stephanie / Kelly, Deanna L

The Psychiatric quarterly

2017 Volume 89, Issue 1, Page(s) 157–168

Abstract: Popular media often portray people with a mental illness as being aggressive, violent, and incarcerated as a result of their behavior. Despite exaggeration in the media, risks for some aggressive behaviors are in fact higher in individuals with ... ...

Abstract	Popular media often portray people with a mental illness as being aggressive, violent, and incarcerated as a result of their behavior. Despite exaggeration in the media, risks for some aggressive behaviors are in fact higher in individuals with schizophrenia. This is often the case with influence of comorbid substance use disorders. It is essential that mental health professionals are aware of treatments that may help with attenuating and treating behaviors that contribute to violence, aggression and incarceration. This paper reviews violence and incarceration in individuals with schizophrenia as well as recommendations, guidelines and benefits for the use of clozapine in this population. Clozapine remains one of the most underutilized evidence-based medications available in the psychiatric arena in the United States. It is a viable and recommended option in the forensic population and it may be helpful on the path to recovery as well as bring substantial savings to the criminal justice system.
MeSH term(s)	Aggression/drug effects ; Antipsychotic Agents/therapeutic use ; Clozapine/therapeutic use ; Criminal Law ; Criminals ; Humans ; Schizophrenia/drug therapy ; Violence/prevention & control
Chemical Substances	Antipsychotic Agents ; Clozapine (J60AR2IKIC)
Language	English
Publishing date	2017-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	207521-0
ISSN	1573-6709 ; 0033-2720
ISSN (online)	1573-6709
ISSN	0033-2720
DOI	10.1007/s11126-017-9521-z
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Article ; Online: Influence of kynurenine 3-monooxygenase (KMO) gene polymorphism on cognitive function in schizophrenia.

Wonodi, Ikwunga / McMahon, Robert P / Krishna, Nithin / Mitchell, Braxton D / Liu, Judy / Glassman, Matthew / Hong, L Elliot / Gold, James M

Schizophrenia research

2014 Volume 160, Issue 1-3, Page(s) 80–87

Abstract: Background: Cognitive deficits compromise quality of life and productivity for individuals with schizophrenia and have no effective treatments. Preclinical data point to the kynurenine pathway of tryptophan metabolism as a potential target for pro- ... ...

Abstract	Background: Cognitive deficits compromise quality of life and productivity for individuals with schizophrenia and have no effective treatments. Preclinical data point to the kynurenine pathway of tryptophan metabolism as a potential target for pro-cognitive drug development. We have previously demonstrated association of a kynurenine 3-monooxygenase (KMO) gene variant with reduced KMO gene expression in postmortem schizophrenia cortex, and neurocognitive endophenotypic deficits in a clinical sample. KMO encodes kynurenine 3-monooxygenase (KMO), the rate-limiting microglial enzyme of cortical kynurenine metabolism. Aberration of the KMO gene might be the proximal cause of impaired cortical kynurenine metabolism observed in schizophrenia. However, the relationship between KMO variation and cognitive function in schizophrenia is unknown. This study examined the effects of the KMO rs2275163C>T C (risk) allele on cognitive function in schizophrenia. Methods: We examined the association of KMO polymorphisms with general neuropsychological performance and P50 gating in a sample of 150 schizophrenia and 95 healthy controls. Results: Consistent with our original report, the KMO rs2275163C>T C (risk) allele was associated with deficits in general neuropsychological performance, and this effect was more marked in schizophrenia compared with controls. Additionally, the C (Arg452) allele of the missense rs1053230C>T variant (KMO Arg452Cys) showed a trend effect on cognitive function. Neither variant affected P50 gating. Conclusions: These data suggest that KMO variation influences a range of cognitive domains known to predict functional outcome. Extensive molecular characterization of this gene would elucidate its role in cognitive function with implications for vertical integration with basic discovery.
MeSH term(s)	Adolescent ; Adult ; Alleles ; Cognition ; Evoked Potentials ; Female ; Genotyping Techniques ; Humans ; Kynurenine 3-Monooxygenase/genetics ; Male ; Middle Aged ; Mutation, Missense ; Neuropsychological Tests ; Polymorphism, Single Nucleotide ; Schizophrenia/genetics ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; Young Adult
Chemical Substances	Kynurenine 3-Monooxygenase (EC 1.14.13.9)
Language	English
Publishing date	2014-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2014.10.026
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Article: Psychopathological and cognitive correlates of tardive dyskinesia in patients treated with neuroleptics.

Wonodi, Ikwunga / Hong, L Elliot / Thaker, Gunvant K

Advances in neurology

2005 Volume 96, Page(s) 336–349

Abstract: Even though new cases of TD are on the decline in North America and other western countries, TD remains a public health concern for patients with chronic schizophrenia, PAD, and for nonpsychiatric patients treated with dopamine receptor antagonists. The ... ...

Abstract	Even though new cases of TD are on the decline in North America and other western countries, TD remains a public health concern for patients with chronic schizophrenia, PAD, and for nonpsychiatric patients treated with dopamine receptor antagonists. The new generation of atypical antipsychotic medications is believed to pose less risk for TD. However, identifying the cognitive and disease-related correlates of TD should equip clinicians with the necessary tools to reduce the prevalence of this iatrogenic movement disorder. No effective treatments for TD are available. This lack of effective therapy is problematic, especially in the few patients in whom the disorder causes functional impairment and other complications, and in whom it may be irreversible.
MeSH term(s)	Affective Disorders, Psychotic/complications ; Affective Disorders, Psychotic/drug therapy ; Akathisia, Drug-Induced/complications ; Akathisia, Drug-Induced/drug therapy ; Antipsychotic Agents/therapeutic use ; Cognition/drug effects ; Humans ; Psychopathology
Chemical Substances	Antipsychotic Agents
Language	English
Publishing date	2005
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	0091-3952
ISSN	0091-3952
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Article: Nicotine effect on prepulse inhibition and prepulse facilitation in schizophrenia patients.

Hong, L Elliot / Wonodi, Ikwunga / Lewis, Jada / Thaker, Gunvant K

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2007 Volume 33, Issue 9, Page(s) 2167–2174

Abstract: Acoustic prepulse inhibition (PPI) is considered an important biomarker in animal studies of psychosis and a number of psychiatric conditions. Nicotine has been shown to improve acoustic PPI in some animal strains and in humans. However, there is little ... ...

Abstract	Acoustic prepulse inhibition (PPI) is considered an important biomarker in animal studies of psychosis and a number of psychiatric conditions. Nicotine has been shown to improve acoustic PPI in some animal strains and in humans. However, there is little data on effects of nicotine on acoustic PPI in schizophrenia patients using a double-blind, placebo-controlled study design. The primary aim of the current study was to test the effect of nicotine nasal spray on acoustic PPI in schizophrenia patients. The secondary aim was to test nicotine effect on prepulse facilitation (PPF). The study included 18 schizophrenia patient smokers and 12 healthy control smokers, tested in a double-blind, placebo-controlled, crossover, randomized design immediately after nicotine or saline placebo nasal sprays. PPI was tested using 120 ms prepulse-pulse interval. PPF was tested using 4500 ms prepulse-pulse interval. The results showed a significant main effect of drug on PPI in that nicotine improved PPI compared to placebo (p=0.008) with no drug by diagnosis interaction (p=0.90). Improvement in PPI in response to nicotine was significantly correlated with the baseline severity of clinical symptoms (r=0.59, p=0.02) in patients. There was no significant drug or drug by diagnosis interaction for the 4500 ms prepulse-pulse interval condition. However, nicotine improved inhibition in a subgroup of subjects exhibiting PPF (p=0.002). In conclusion, the findings confirmed that nicotine transiently improves acoustic PPI in schizophrenia patients. Additionally, schizophrenia patients with more clinical symptoms may have benefited more from nicotinic effect on PPI.
MeSH term(s)	Acoustic Stimulation/methods ; Adult ; Analysis of Variance ; Chi-Square Distribution ; Female ; Humans ; Inhibition, Psychological ; Male ; Middle Aged ; Nicotine/pharmacology ; Nicotinic Agonists/pharmacology ; Psychiatric Status Rating Scales ; Reaction Time/drug effects ; Reflex, Acoustic/drug effects ; Reflex, Acoustic/radiation effects ; Reflex, Startle/drug effects ; Schizophrenia/physiopathology ; Schizophrenic Psychology
Chemical Substances	Nicotinic Agonists ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2007-10-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/sj.npp.1301601
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Article ; Online: Evidence of missense mutations on the neuregulin 1 gene affecting function of prepulse inhibition.

Hong, L Elliot / Wonodi, Ikwunga / Stine, O Colin / Mitchell, Braxton D / Thaker, Gunvant K

Biological psychiatry

2008 Volume 63, Issue 1, Page(s) 17–23

Abstract: Background: Neuregulin 1 (NRG1) is one of the leading candidate genes in schizophrenia. Rodents with NRG1 knock-out showed significantly impaired prepulse inhibition (PPI) in the original report linking NRG1 to schizophrenia. A widely used surrogate ... ...

Abstract	Background: Neuregulin 1 (NRG1) is one of the leading candidate genes in schizophrenia. Rodents with NRG1 knock-out showed significantly impaired prepulse inhibition (PPI) in the original report linking NRG1 to schizophrenia. A widely used surrogate measure of psychosis in animal models, PPI is considered a schizophrenia endophenotype. We hypothesized that if NRG1 influences PPI in rodents, then it should have a similar effect on PPI in humans. Methods: We examined the potential neurophysiological effects of two nonsynonymous single nucleotide polymorphisms located on NRG1 (rs3924999 and rs10503929) on PPI. Genotyping was completed in 430 unrelated individuals, including 244 schizophrenia cases and 186 controls. PPI was available in a subgroup of 113 cases and 63 controls. Results: Rs3924999 genotype was significantly associated with PPI (p = .003): PPI was lowest in the subjects who were homozygous for the minor allele A/A carriers, intermediate in A/G carriers, and highest in homozygous major alleles G/G carriers. The associations persisted within cases (p = .02) and controls (p = .02) analyzed separately. An additive model suggested that rs3924999 alone contributes to 7.9% of the PPI variance. In contrast, rs10503929 genotype was not associated with PPI (p = .85). Schizophrenia patients had reduced PPI compared to control subjects (p = .04). Neither single nucleotide polymorphism was associated with schizophrenia (all p > .37). However, schizophrenia patients with abnormal PPI may be associated with rs3924999 (p = .05). Conclusions: A missense mutation on rs3924999 of the neuregulin 1 gene may have a functional effect on prepulse inhibition in both schizophrenia and healthy control populations.
MeSH term(s)	Adolescent ; Adult ; Aged ; Alleles ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Humans ; Inhibition (Psychology) ; Male ; Middle Aged ; Mutation, Missense ; Neuregulin-1/genetics ; Reflex, Startle/genetics ; Schizophrenia/genetics ; Schizophrenia/physiopathology ; Schizophrenic Psychology
Chemical Substances	Neuregulin-1
Language	English
Publishing date	2008-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2007.05.011
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Article ; Online: Dipyridamole monotherapy in schizophrenia: pilot of a novel treatment approach by modulation of purinergic signaling.

Wonodi, Ikwunga / Gopinath, Hirekatur V / Liu, Judy / Adami, Helene / Hong, L Elliot / Allen-Emerson, Robert / McMahon, Robert P / Thaker, Gunvant K

Psychopharmacology

2011 Volume 218, Issue 2, Page(s) 341–345

Abstract: Background: Emerging data indicate the neuromodulator adenosine may play a role in the therapeutics of schizophrenia. Adenosine A(2A) receptor stimulation exerts a functional antagonism at postsynaptic D(2) receptors. Data from animal models relevant to ...

Abstract	Background: Emerging data indicate the neuromodulator adenosine may play a role in the therapeutics of schizophrenia. Adenosine A(2A) receptor stimulation exerts a functional antagonism at postsynaptic D(2) receptors. Data from animal models relevant to schizophrenia support a therapeutic effect of modulating adenosinergic transmission in the ventral striatum. One previous clinical trial showed superiority of adjunctive dipyridamole, an adenosine reuptake inhibitor, compared to placebo in ameliorating positive symptoms in schizophrenia patients. Objectives: The aim of this study was to examine the effects of dipyridamole monotherapy of 200 mg/day on positive and negative symptoms, with the goal of determining dosing for future adjunctive studies in schizophrenia. Methods: Twenty symptomatic schizophrenia participants were randomized to a 6-week double-blind trial comparing olanzapine (20 mg/day) to dipyridamole monotherapy (200 mg/day). Thirteen participants completed the treatment phase (eight on dipyridamole; five on olanzapine). Results: The olanzapine group showed a trend (p = 0.08) for superiority on BPRS total scores (mean ± SD: total BPRS score decreasing from 36.8 ± 2.3 at week 1, to 33.2 ± 5.5 at the end of the study). The mean total BPRS scores decreased from 36.4 ± 5.3 to 34.0 ± 7.7 in the dipyridamole group. Conclusions: Although these pilot data do not support a significant antipsychotic effect of dipyridamole monotherapy, the results provide some evidence for examining dipyridamole (200 mg/day) as adjunct to symptomatic antipsychotic-treated schizophrenia patients.
MeSH term(s)	Adolescent ; Adult ; Antipsychotic Agents/therapeutic use ; Benzodiazepines/therapeutic use ; Brief Psychiatric Rating Scale ; Dipyridamole/pharmacology ; Dipyridamole/therapeutic use ; Double-Blind Method ; Follow-Up Studies ; Humans ; Middle Aged ; Olanzapine ; Phosphodiesterase Inhibitors/pharmacology ; Phosphodiesterase Inhibitors/therapeutic use ; Pilot Projects ; Schizophrenia/drug therapy ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; Treatment Outcome ; Young Adult
Chemical Substances	Antipsychotic Agents ; Phosphodiesterase Inhibitors ; Benzodiazepines (12794-10-4) ; Dipyridamole (64ALC7F90C) ; Olanzapine (N7U69T4SZR)
Language	English
Publishing date	2011-05-03
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-011-2315-3
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Article: Independent domains of inhibitory gating in schizophrenia and the effect of stimulus interval.

Hong, L Elliot / Summerfelt, Ann / Wonodi, Ikwunga / Adami, Helene / Buchanan, Robert W / Thaker, Gunvant K

The American journal of psychiatry

2007 Volume 164, Issue 1, Page(s) 61–65

Abstract: Objective: Patients with schizophrenia are known to have inhibitory gating deficits in the suppression of evoked potential P50 response to repeated stimuli and the prepulse inhibition of the startle response. In the current study, the authors aimed to ... ...

Abstract	Objective: Patients with schizophrenia are known to have inhibitory gating deficits in the suppression of evoked potential P50 response to repeated stimuli and the prepulse inhibition of the startle response. In the current study, the authors aimed to determine whether these two inhibitory gating measures are related in schizophrenia patients or whether abnormal P50 suppression and abnormal prepulse inhibition are independent neurophysiological characteristics of schizophrenia. The authors hypothesized that the relationship of the two measures may vary as a function of interstimulus intervals of stimulus presentations. Method: Fifty-nine schizophrenia patients and 17 healthy comparison subjects were tested on both P50 suppression and prepulse inhibition. P50 suppression was measured using paired clicks with 500-msec interstimulus intervals. Prepulse inhibition was measured by using a series of prepulse-pulse pairs with interstimulus intervals ranging from 30 to 500 msec. Results: Patients showed reduced P50 suppression and prepulse inhibition in relation to healthy comparison subjects. Concordance analysis showed that abnormal P50 suppression and abnormal prepulse inhibition do not necessarily occur together. Prepulse inhibition was most prominent at the 120-msec interstimulus interval, which was not correlated to P50 suppression. At the 500-msec interstimulus interval, prepulse inhibition was significantly but negatively correlated to P50 suppression. Prepulse inhibition at the other interstimulus intervals was not correlated with P50 suppression. Conclusions: These neurophysiological measures lack robust and direct relationships and likely mark independent aspects of abnormal brain inhibitory functions in schizophrenia.
MeSH term(s)	Acoustic Stimulation ; Adolescent ; Adult ; Aged ; Ambulatory Care ; Brain/physiopathology ; Electroencephalography/statistics & numerical data ; Evoked Potentials, Auditory/physiology ; Female ; Habituation, Psychophysiologic/physiology ; Humans ; Male ; Middle Aged ; Neural Inhibition/physiology ; Reflex, Startle/physiology ; Schizophrenia/diagnosis ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; Time Factors
Language	English
Publishing date	2007-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	280045-7
ISSN	1535-7228 ; 0002-953X
ISSN (online)	1535-7228
ISSN	0002-953X
DOI	10.1176/ajp.2007.164.1.61
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Article ; Online: Impaired kynurenine pathway metabolism in the prefrontal cortex of individuals with schizophrenia.

Sathyasaikumar, Korrapati V / Stachowski, Erin K / Wonodi, Ikwunga / Roberts, Rosalinda C / Rassoulpour, Arash / McMahon, Robert P / Schwarcz, Robert

Schizophrenia bulletin

2010 Volume 37, Issue 6, Page(s) 1147–1156

Abstract: The levels of kynurenic acid (KYNA), an astrocyte-derived metabolite of the branched kynurenine pathway (KP) of tryptophan degradation and antagonist of α7 nicotinic acetylcholine and N-methyl-D-aspartate receptors, are elevated in the prefrontal cortex ( ...

Abstract	The levels of kynurenic acid (KYNA), an astrocyte-derived metabolite of the branched kynurenine pathway (KP) of tryptophan degradation and antagonist of α7 nicotinic acetylcholine and N-methyl-D-aspartate receptors, are elevated in the prefrontal cortex (PFC) of individuals with schizophrenia (SZ). Because endogenous KYNA modulates extracellular glutamate and acetylcholine levels in the PFC, these increases may be pathophysiologically significant. Using brain tissue from SZ patients and matched controls, we now measured the activity of several KP enzymes (kynurenine 3-monooxygenase [KMO], kynureninase, 3-hydroxyanthranilic acid dioxygenase [3-HAO], quinolinic acid phosphoribosyltransferase [QPRT], and kynurenine aminotransferase II [KAT II]) in the PFC, ie, Brodmann areas (BA) 9 and 10. Compared with controls, the activities of KMO (in BA 9 and 10) and 3-HAO (in BA 9) were significantly reduced in SZ, though there were no significant differences between patients and controls in kynureninase, QPRT, and KAT II. In the same samples, we also confirmed the increase in the tissue levels of KYNA in SZ. As examined in rats treated chronically with the antipsychotic drug risperidone, the observed biochemical changes were not secondary to medication. A persistent reduction in KMO activity may have a particular bearing on pathology because it may signify a shift of KP metabolism toward enhanced KYNA synthesis. The present results further support the hypothesis that the normalization of cortical KP metabolism may constitute an effective new treatment strategy in SZ.
MeSH term(s)	Adult ; Aged ; Animals ; Antipsychotic Agents/pharmacology ; Case-Control Studies ; Female ; Humans ; Kynurenine/metabolism ; Kynurenine 3-Monooxygenase/metabolism ; Male ; Metabolic Networks and Pathways/drug effects ; Middle Aged ; Oxidoreductases/metabolism ; Pentosyltransferases/metabolism ; Postmortem Changes ; Prefrontal Cortex/metabolism ; Rats ; Rats, Sprague-Dawley ; Risperidone/pharmacology ; Schizophrenia/metabolism ; Transaminases/metabolism
Chemical Substances	Antipsychotic Agents ; Kynurenine (343-65-7) ; Oxidoreductases (EC 1.-) ; 3-hydroxyanthranilic acid oxidase (EC 1.10.3.5) ; Kynurenine 3-Monooxygenase (EC 1.14.13.9) ; Pentosyltransferases (EC 2.4.2.-) ; nicotinate-nucleotide diphosphorylase (carboxylating) (EC 2.4.2.19) ; Transaminases (EC 2.6.1.-) ; kynurenine-oxoglutarate transaminase (EC 2.6.1.7) ; Risperidone (L6UH7ZF8HC)
Language	English
Publishing date	2010-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	439173-1
ISSN	1745-1701 ; 0586-7614
ISSN (online)	1745-1701
ISSN	0586-7614
DOI	10.1093/schbul/sbq112
Database	MEDical Literature Analysis and Retrieval System OnLINE

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