Associações entre neurocognição, cognição social e estresse oxidativo na esquizofrenia

• Ano de defesa: 2017
• Autor(a) principal: Breno Fiuza Cruz
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Desempenho Funcional; Memória de Trabalho; Esquizofrenia; Validação; Cognição Social; Estresse Oxidativo; Neurocognição; Memória de curto prazo; Neurociências; Cognição; Estresse oxidativo
• Link de acesso: http://hdl.handle.net/1843/BUOS-B49MYR

INTRODUCTION: Schizophrenia is a severe and incapacitating mental disorder of unknown etiology that does not have completely effective treatments for all dimensions of the disorder. Deficits in neurocognition and social cognition play a fundamental role in the functional impairment of the disease. A possible contribution to the pathophysiology of the disorder seems to be due to oxidative stress, which impairs neuronal function, especially of GABAergic parvalbumin interneurons (PVIs) and NMDA receptors. This dysfunction can lead to impairments in neurocognitive function (especially working memory) and social cognition. OBJECTIVES: to analyze deficits in neurocognition and social cognition and their relationships with oxidative stress. To contribute with the validation of two scales that evaluate social cognition. MATERIAL AND METHODS: 104 stable patients living in the community diagnosed with schizophrenia and 89 controls were evaluated. Neurocognition was evaluated through the Brief Assessment of Cognition in Schizophrenia (BACS). Social cognition was assessed through a test of Theory of Mind (Hinting Task) and an emotion processing test (Recognition of Facial Expressions -RFE). Functional ability was assessed using the UCSD Performance-based Skills Assessment (UPSA). Oxidative stress was assessed by measuring serum levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS). Simple correlations were made between the variables studied, as well as multiple linear regressions to establish the determinants of social cognition, functional capacity and working memory. RESULTS: There is a statistically significant difference between patients and controls regarding neurocognition and social cognition (Hinting Task Z=6,85; p<0,001. RFE t=4,88; p<0,001), as well as serum level of GSH (Z=3,56; p<0,001) and TBARS (Z=5,51; P<0,001). The main predictors of variation in social cognition were neurocognitive domains. Social cognition explains an additional variation of 18% beyond neurocognition regarding functional capacity. Higher serum level of TBARS in patients was associated with poorer performance in the working memory test (r=-0,39; p=0,002) and no other cognitive domain. Oxidative stress is more relevant to performance in working memory test (Standard Beta: -0,36; CI= -2,52 a -13,71) than age and negative symptoms. Higher level of TBARS correlated with worse performance in the Hinting Task (Theory of Mind) in healthy controls (rho=-,036; p=0,038, after Bonferroni correction for multiple correlations). DISCUSSION AND CONCLUSION: The relationships between neurocognition, social cognition and functional capacity found in this study are supported by the literature. The validity of the tests that evaluate the social cognition can be determined, since the relation of these tests with other clinical variables is similar to the one observed in the literature. The relationship between greater lipid peroxidation measured by TBARS and worse performance in working memory is compatible with the theoretical models of greater vulnerability of PVIs to oxidative stress