TY - JOUR
T1 - Investigating potential associations between neurocognition/social cognition and oxidative stress in schizophrenia
AU - Cruz, Breno Fiuza
AU - de Campos-Carli, Salvina Maria
AU - de Oliveira, Amanda Margarida
AU - de Brito, Camila Bernardo
AU - Garcia, Zélia Menezes
AU - Duque do Arifa, Raquel Nascimento
AU - de Souza, Daniele da Glória
AU - Teixeira, Antonio Lucio
AU - Salgado, João Vinícius
N1 - Publisher Copyright:
© 2021
PY - 2021/4
Y1 - 2021/4
N2 - Introduction: Deficits in neurocognition and social cognition play a critical role in the functional impairment of patients with schizophrenia. Increased oxidative stress has been evidenced in schizophrenia. Increased oxidative stress can affect neuronal function and lead to impairments in neurocognitive functions (especially working memory) and social cognition. Objective: To investigate deficits in neurocognition and social cognition and their potential association with oxidative stress biomarkers in schizophrenia. Material and methods: Eight-five clinically stable patients with schizophrenia and 75 controls were enrolled in this study. Neurocognition was evaluated through the Brief Assessment of Cognition in Schizophrenia (BACS). Social cognition was assessed through the Hinting Task – a test of theory of mind – and an emotion processing test, Facial Emotion Recognition Test (FERT-100). Oxidative stress was assessed by measuring serum levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS). Results: Patients had decreased serum levels of GSH (Z=3.56; p<0.001) and increased TBARS (Z=5.51; P<0.001) when compared with controls. TBARS levels are higher in patients using first generation antipsychotics. Higher serum levels of TBARS in patients were associated with poor performance in working memory test (r=-0.39; p=0.002), even when controlling for age and negative symptoms (Standard Beta: -0.36; CI= -2.52 a -13.71). Discussion: The association between greater lipid peroxidation, as assessed by TBARS, and worse performance in working memory corroborates theoretical models of greater vulnerability of schizophrenia to oxidative stress.
AB - Introduction: Deficits in neurocognition and social cognition play a critical role in the functional impairment of patients with schizophrenia. Increased oxidative stress has been evidenced in schizophrenia. Increased oxidative stress can affect neuronal function and lead to impairments in neurocognitive functions (especially working memory) and social cognition. Objective: To investigate deficits in neurocognition and social cognition and their potential association with oxidative stress biomarkers in schizophrenia. Material and methods: Eight-five clinically stable patients with schizophrenia and 75 controls were enrolled in this study. Neurocognition was evaluated through the Brief Assessment of Cognition in Schizophrenia (BACS). Social cognition was assessed through the Hinting Task – a test of theory of mind – and an emotion processing test, Facial Emotion Recognition Test (FERT-100). Oxidative stress was assessed by measuring serum levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS). Results: Patients had decreased serum levels of GSH (Z=3.56; p<0.001) and increased TBARS (Z=5.51; P<0.001) when compared with controls. TBARS levels are higher in patients using first generation antipsychotics. Higher serum levels of TBARS in patients were associated with poor performance in working memory test (r=-0.39; p=0.002), even when controlling for age and negative symptoms (Standard Beta: -0.36; CI= -2.52 a -13.71). Discussion: The association between greater lipid peroxidation, as assessed by TBARS, and worse performance in working memory corroborates theoretical models of greater vulnerability of schizophrenia to oxidative stress.
KW - Neurocognition
KW - Oxidative stress
KW - Schizophrenia
KW - Social cognition
KW - Working memory
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U2 - 10.1016/j.psychres.2021.113832
DO - 10.1016/j.psychres.2021.113832
M3 - Article
C2 - 33652247
AN - SCOPUS:85101648865
SN - 0165-1781
VL - 298
JO - Psychiatry Research
JF - Psychiatry Research
M1 - 113832
ER -