Plasmaβ-III tubulin, neurofilament light chain and glial fibrillary acidic protein are associated with neurodegeneration and progression in schizophrenia
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Identificadores
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Visualización o descarga de ficheros
Fecha de publicación
2020Título de revista
Scientific Reports
Tipo de contenido
Journal Article
DeCS
proteína ácida fibrilar de la glía | estudios de casos y controles | encéfalo | antipsicóticos | proteínas de neurofilamentos | humanos | escalas de valoración psiquiátrica | adulto | tubulina (proteína) | progresión de la enfermedad | esquizofreniaMeSH
Schizophrenia | Glial Fibrillary Acidic Protein | Neurofilament Proteins | Adult | Humans | Tubulin | Psychiatric Status Rating Scales | Brain | Case-Control Studies | Disease Progression | Antipsychotic AgentsResumen
Schizophrenia is a progressive disorder characterized by multiple psychotic relapses. After every relapse, patients may not fully recover, and this may lead to a progressive loss of functionality. Pharmacological treatment represents a key factor to minimize the biological, psychological and psychosocial impact of the disorder. The number of relapses and the duration of psychotic episodes induce a potential neuronal damage and subsequently, neurodegenerative processes. Thus, a comparative study was performed, including forty healthy controls and forty-two SZ patients divided into first-episode psychosis (FEP) and chronic SZ (CSZ) subgroups, where the CSZ sub group was subdivided by antipsychotic treatment. In order to measure the potential neuronal damage, plasma levels of beta-III tubulin, neurofilament light chain (Nf-L), and glial fibrillary acidic protein (GFAP) were performed. The results revealed that the levels of these proteins were increased in the SZ group compared to the control group (P < 0.05). Moreover, multiple comparison analysis showed highly significant levels of beta-III tubulin (P = 0.0002), Nf-L (P = 0.0403) and GFAP (P < 0.015) in the subgroup of CSZ clozapine-treated. In conclusion, beta-III tubulin, Nf-L and GFAP proteins may be potential biomarkers of neurodegeneration and progression in SZ.