Schizophrenia (SCZ) is a severe psychiatric disorder with several clinical manifestations that include cognitive dysfunction, decline in motivation, and psychosis. Current standards of care treatment with antipsychotic agents are often ineffective in controlling the disease, as only one-third of SCZ patients respond to medications. The mechanisms underlying the pathogenesis of SCZ remain elusive. It is believed that inflammatory processes may play a role as contributing factors to the etiology of SCZ. Galectins are a family of β-galactoside-binding lectins that contribute to the regulation of immune and inflammatory responses, and previous reports have shown their role in the maintenance of central nervous system (CNS) homeostasis and neuroinflammation. In the current study, we evaluated the expression levels of the galectin gene family in post-mortem samples of the hippocampus, associative striatum, and dorsolateral prefrontal cortex from SCZ patients. We found a significant downregulation of () in the hippocampus of SCZ patients as compared to otherwise healthy donors. Interestingly, the reduction of was disease-specific, as no modulation was observed in the hippocampus from bipolar nor major depressive disorder (MDD) patients. Prediction analysis identified TBL1XR1, BRF2, and TAF7 as potential transcription factors controlling expression. In addition, MIR3681HG and MIR4296 were negatively correlated with expression, suggesting a role for epigenetics in the regulation of levels. On the other hand, no differences in the methylation levels of were observed between SCZ and matched control hippocampus. Finally, ontology analysis of the genes negatively correlated with expression identified an enrichment of the NGF-stimulated transcription pathway and of the oligodendrocyte differentiation pathway. Our study identified as a disease-specific gene, characterizing SCZ patients, that may in the future be exploited as a potential therapeutic target.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8392448PMC
http://dx.doi.org/10.3390/brainsci11080973DOI Listing

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