Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

A Generalized Cognitive Decline (GCoDe) Partly Mediates the Effects of Neuro-Immune and Neuro-Oxidative Toxicity on the Symptomatome and Lowered Quality of Life in (Deficit) Schizophrenia

Version 1 : Received: 19 November 2020 / Approved: 19 November 2020 / Online: 19 November 2020 (21:06:35 CET)

How to cite: Maes, M.; Kanchanatawan, B. A Generalized Cognitive Decline (GCoDe) Partly Mediates the Effects of Neuro-Immune and Neuro-Oxidative Toxicity on the Symptomatome and Lowered Quality of Life in (Deficit) Schizophrenia. Preprints 2020, 2020110523 (doi: 10.20944/preprints202011.0523.v1). Maes, M.; Kanchanatawan, B. A Generalized Cognitive Decline (GCoDe) Partly Mediates the Effects of Neuro-Immune and Neuro-Oxidative Toxicity on the Symptomatome and Lowered Quality of Life in (Deficit) Schizophrenia. Preprints 2020, 2020110523 (doi: 10.20944/preprints202011.0523.v1).

Abstract

Recently we showed that schizophrenia and, especially, deficit schizophrenia is accompanied by neurocognitive impairments as measured with different cognitive batteries. The aim of this study was to examine whether a single trait underpins aberrations in 9 key Cambridge Neuropsychological Test Automated Battery (CANTAB) probes, verbal fluency (VFT), world list memory (WLM), true recall, and the Mini Mental State Examination (MMSE). We recruited 80 patients with schizophrenia and 40 healthy controls. All patients were assessed using CANTAB tests, namely paired-association learning (PAL), rapid visual information (RVP), spatial working memory (SWM), one touch stocking (OTS), intra/extradimensional set shifting (IED), and emotional recognition test (ERT). We found that a single latent trait, which is essentially unidimensional, underlies the CANTAB tests, VFT, WLM, True Recall and MMSE. The latent trait shows excellent psychometric properties and fits a reflective model and, therefore, reflects a generalized cognitive decline (GCoDe), which is the cause of aberrations in semantic and episodic memory, recall, executive functions, strategy use, rule acquisition, visual sustained attention, attention set-shifting and emotional recognition. 40.5% of the variance in GCode was explained by CCL11, IgA to tryptophan catabolites, and increased oxidative toxicity. GCoDe explains 44.8% of the variance in a single latent trait extracted from psychosis, hostility, excitation, mannerism, negative symptoms, formal thought disorders, and psychomotor retardation and 40.9% in quality of life scores. GCoDe is significantly greater in deficit than in nondeficit schizophrenia. In conclusion, GCoDe mediates the effects of neuro-immune and neuro-oxidative toxicity on the phenome of (deficit) schizophrenia.

Subject Areas

deficit schizophrenia; cognition; tryptophan catabolites; neuro-immune; oxidative stress; antioxidants; CCL11

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