Abstract
Schizophrenia is a severe psychiatric illness that affects millions of people globally, generates large health expenses and deprives patients of a normal life. The diagnosis is clinical and the only way of managing the symptoms is using psychosocial interventions and antipsychotic drugs, which have negative side effects. These drugs are classified into two categories: typical (first-generation) and atypical (second-generation), and its combination with D-serine (an endogenous glutamatergic N-methyl-D-aspartate (NMDA) receptor co-agonist) seems to improve the relief of symptoms. Proteomic studies have associated the development and establishment of schizophrenia to dysfunctions in neurotransmitter systems and oligodendrocytes. The dysfunction of these cells may lead to disturbances in myelination, and consequently to a poor propagation of nerve impulses, compromising cognitive, neural and glial functions. In this context, this project aims to identify the proteins and pathways affected in MO3.13 (a human oligodendrocyte lineage) by the use of haloperidol (first-generation antipsychotic), clozapine (second-generation antipsychotic) and D-serine, through total proteome analyses.
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