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Abstract
Aim & Objective: To delineate the associations between executive impairments and changes in tryptophan catabolite (TRYCAT) patterning, negative symptoms and deficit schizophrenia.
Methods: We recruited 80 schizophrenic patients and 40 healthy controls and assessed 10 key cognitive tests using the Cambridge Neuropsychological Test Automated Battery (CANTAB), IgA/IgM responses to tryptophan catabolites (TRYCATs), the Scale for the Assessment of Negative Symptoms (SANS) and Positive and Negative Syndrome Scale.
Results: Partial Least Squares path modeling shows that a large part of the variance in negative symptoms and the deficit phenotype (39-53%) is explained by executive impairments, TRYCAT levels and male sex and that 53.4% of the variance in executive impairments is explained by TRYCATs, lower education, age and a familial history of psychosis. Specific indirect effects of TRYCATs, age and education on negative symptoms are mediated by executive impairments. Nevertheless, sustained attention, memory and emotion recognition also mediate the effects of TRYCATS, lower education and male sex on negative symptoms.
Conclusion: Deficit schizophrenia is accompanied by a broader spectrum of cognitive impairments than nondeficit schizophrenia, including executive functions, sustained attention, episodic and semantic memory and emotion recognition. Furthermore, neuro-immune disorders underpin executive impairments, whilst neuro-immune disorders coupled with executive and other cognitive impairments to a large extent determine negative symptoms and the deficit phenotype.
Keywords: Deficit schizophrenia, negative symptoms, cognition, neuro-immune, inflammation, oxidative stress.
CNS & Neurological Disorders - Drug Targets
Title:The Effects of Tryptophan Catabolites on Negative Symptoms and Deficit Schizophrenia are Partly Mediated by Executive Impairments: Results of Partial Least Squares Path Modeling
Volume: 17 Issue: 6
Author(s): Buranee Kanchanatawan and Michael Maes*
Affiliation:
- Faculty of Medicine, Department of Psychiatry, Chulalongkorn University, Patumwan, Bangkok, 10330,Thailand
Keywords: Deficit schizophrenia, negative symptoms, cognition, neuro-immune, inflammation, oxidative stress.
Abstract: Aim & Objective: To delineate the associations between executive impairments and changes in tryptophan catabolite (TRYCAT) patterning, negative symptoms and deficit schizophrenia.
Methods: We recruited 80 schizophrenic patients and 40 healthy controls and assessed 10 key cognitive tests using the Cambridge Neuropsychological Test Automated Battery (CANTAB), IgA/IgM responses to tryptophan catabolites (TRYCATs), the Scale for the Assessment of Negative Symptoms (SANS) and Positive and Negative Syndrome Scale.
Results: Partial Least Squares path modeling shows that a large part of the variance in negative symptoms and the deficit phenotype (39-53%) is explained by executive impairments, TRYCAT levels and male sex and that 53.4% of the variance in executive impairments is explained by TRYCATs, lower education, age and a familial history of psychosis. Specific indirect effects of TRYCATs, age and education on negative symptoms are mediated by executive impairments. Nevertheless, sustained attention, memory and emotion recognition also mediate the effects of TRYCATS, lower education and male sex on negative symptoms.
Conclusion: Deficit schizophrenia is accompanied by a broader spectrum of cognitive impairments than nondeficit schizophrenia, including executive functions, sustained attention, episodic and semantic memory and emotion recognition. Furthermore, neuro-immune disorders underpin executive impairments, whilst neuro-immune disorders coupled with executive and other cognitive impairments to a large extent determine negative symptoms and the deficit phenotype.
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Cite this article as:
Kanchanatawan Buranee and Maes Michael *, The Effects of Tryptophan Catabolites on Negative Symptoms and Deficit Schizophrenia are Partly Mediated by Executive Impairments: Results of Partial Least Squares Path Modeling, CNS & Neurological Disorders - Drug Targets 2018; 17 (6) . https://dx.doi.org/10.2174/1871527317666180702160921
DOI https://dx.doi.org/10.2174/1871527317666180702160921 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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