Recently, specific immunometabolic profiles have been postulated in patients with schizophrenia, even before full-blown disease and independent of antipsychotic treatment. Proteomic profiling studies offer a promising potential for elucidating the cellular and molecular pathways that may be involved in the onset and progression of schizophrenia symptoms, and co-occurrent metabolic changes. In view of all this, we were intrigued to explore galectin-3 (Gal-3) as a glycan, and in our previous study, we measured its elevated levels in remission of schizophrenia. The finding may be a consequence of antipsychotic treatment and may have an impact on the onset of inflammation, the development of obesity, and the presumed cognitive changes in schizophrenia. In the animal study, it was shown that downregulation of Gal-3 was beneficial in insulin regulation of obesity and cognitive preservation. Strategies involving plasma exchange are discussed in this review, particularly in the context of Gal-3 elimination.
Keywords: Antipsychotics; Cognition; Galectin-3; Insulin resistance; Metabolic syndrome; Schizophrenia.
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