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.