Evidence map›Paper›PMID 28875464›Full record

ArticleMolecular neurobiology2018

Changes in Tryptophan Catabolite (TRYCAT) Pathway Patterning Are Associated with Mild Impairments in Declarative Memory in Schizophrenia and Deficits in Semantic and Episodic Memory Coupled with Increased False-Memory Creation in Deficit Schizophrenia.

Buranee Kanchanatawan, Solaphat Hemrungrojn, Supaksorn Thika, Sunee Sirivichayakul, Kiat Ruxrungtham, André F Carvalho, Michel Geffard, George Anderson, Michael Maes

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03788759 (Alpha-lipoic Acid Adjunctive Therapy in Schizophrenia), which is not on this map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
6.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03788759 phase2 / phase3completednot on this mapstarted 2019, after this paper: background citation

Alpha-lipoic Acid Adjunctive Therapy in Schizophrenia: A Randomized, Double-blind, Placebo-controlled Trial

TypeinterventionalSponsorNucleo De Pesquisa E Desenvolvimento De Medicamentos Da Universidade Federal Do CearaRan2019 to 2021Enrolled48ConditionsSchizophrenia, Oxidative StressArmsAlpha-lipoic acid, Placebo Oral Tablet
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

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  4. One-day tropisetron treatment improves cognitive deficits and P50 inhibition deficits in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 6 countries.

Buranee KanchanatawanDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Solaphat HemrungrojnDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Supaksorn ThikaDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Sunee SirivichayakulDivision of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Kiat RuxrungthamDivision of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
André F CarvalhoDepartment of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.
Michel GeffardResearch Department, IDRPHT, Talence, France.
George AndersonCRC Scotland & London, Eccleston Square, London, UK.
Michael MaesDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.ORCID http://orcid.org/0000-0002-2012-871X
Chulalongkorn University · THDeakin University · AUInstitut Génétique Nantes Atlantique · FRUniversidade Federal do Ceará · BR

Funding

Asahi Glass Foundation NA
6 · The paper itself

Abstract

Evidence indicates that schizophrenia and in particular negative symptoms and deficit schizophrenia are accompanied by neurocognitive impairments and changes in the patterning of the tryptophan catabolite (TRYCAT) pathway. This cross-sectional study was carried out to examine the associations between cognitive functions (as measured with Consortium to Establish a Registry for Alzheimer's disease (CERAD)) and TRYCAT pathway patterning in patients with (n = 40) and without (n = 40) deficit schizophrenia and normal controls (n = 40). Cognitive measures were assessed with the Verbal Fluency Test (VFT), Boston Naming Test (BNT), Mini-Mental State Examination (MMSE), Word List Memory (WLM), Constructional Praxis, Word List Recall (WLRecall), and Word List Recognition (WLRecognition), while TRYCAT measurements assessed the IgA/IgM responses to noxious TRYCATs, namely quinolinic acid (QA), 3-OH-kynurenine (3HK), picolinic acid (PA), and xanthurenic (XA) acid, and more protective (PRO) TRYCATs, including kynurenic acid (KA) and anthranilic acid (AA). IgA NOX/PRO, IgM KA/3HK, and IgA/IgM NOX/PRO ratios were computed. Schizophrenia was accompanied by lower VFT and WLM, while BNT (dysnomia) and MMSE are significantly lower in multiple- than first-episode schizophrenia. Deficit schizophrenia is strongly associated with worse outcomes on VFT, MMSE, WLM, WLRecall, WLRecognition, and delayed recall savings and increased false memories. Around 40-50% of the variance in negative symptoms' scores was explained by VFT, WLM, WLRecall, and MMSE. Increases in IgA NOX/PRO, IgM KA/3HK, and/or IgA/IgM NOX/PRO ratios were associated with impairments in VFT, BNT, MMSE, WLM, WLRecall, WLRecognition, and false-memory creation. In conclusion, nondeficit schizophrenia is accompanied by mild memory impairments, while disease progression is accompanied by broader cognitive impairments. Deficit schizophrenia and negative symptoms are strongly associated with deficits in working memory, delayed recall and recognition, and increased false-memory creation. These cognitive impairments and memory deficits are in part explained by increased production and/or attenuated regulation of TRYCATs with neurotoxic, excitotoxic, immune-inflammatory, oxidative, and nitrosative potential, which may contribute to neuroprogression.

Indexed as

Memory, EpisodicSemanticsAdultCase-Control StudiesFemaleHumansLinear ModelsMaleMemory DisordersMultivariate AnalysisNeuropsychological TestsSchizophreniaTryptophanTryptophanCompensatory anti-inflammatory reflex systemCytokinesImmune activationInflammationSchizophreniaTryptophan

Identifiers

PMID28875464
OpenAlexW2752675815

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.