Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/14052
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dc.contributor.authorBorovcanin, Milica-
dc.contributor.authorRadosavljevic, Gordana-
dc.contributor.authorPantic, Jelena-
dc.contributor.authorMilovanovic, Jelena-
dc.contributor.authorMijailovic, Natasa-
dc.contributor.authorArsenijevic A.-
dc.contributor.authorArsenijevic, Nebojsa-
dc.date.accessioned2022-02-02T17:54:36Z-
dc.date.available2022-02-02T17:54:36Z-
dc.date.issued2021-01-01-
dc.identifier.issn15680266-
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/14052-
dc.description.abstractThe role of the Galectin-3 (Gal-3) has already been explored in various somatic diseas-es, considering its engagement in infection, acute and chronic inflammation, and autoimmunity. Additionally, it has been recognized that Gal-3 is included in neuroinflammation and neurodegener-ation, 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 schizophrenia.-
dc.relation.ispartofCurrent Topics in Medicinal Chemistry-
dc.titleContrasting roles of the galectin-3 in the schizophrenia onset, clinical presentation, and somatic comorbidity-
dc.typereview-
dc.identifier.doi10.2174/1568026621666210611162420-
dc.identifier.scopus85116328168-
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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