The role of the Galectin-3 (Gal-3) has already been explored in various somatic diseases,
considering its engagement in infection, acute and chronic inflammation, and autoimmunity.
Additionally, it has been recognized that Gal-3 is included in neuroinflammation and neurodegeneration,
so we presented the possibility for its involvement in neuroprogression in schizophrenia.
Gal-3 possibly participates in the early life programming of schizophrenia, also in the specific response
to viral infections as a “second hit” later in life, and as a part of a unique systemic somatic
dysfunction leading to the specific mental changes. In this review, we would like to put all these
previous observations of Gal-3 properties in the context of schizophrenia onset, clinical symptoms
presentation, frequent somatic comorbid states, and future options for Gal-3 centered treatment in