Correlação entre desempenho cognitivo e componentes do sistema endocanabinóide em linfócitos periféricos de pacientes com esquizofrenia e controles

• Ano de defesa: 2013
• Autor(a) principal: Rodrigo Ferretjans Alves
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Fisiopatologia; Cannabis; Esquizofrenia; Sistema imune; Cognição; Déficits cognitivos; Sistema endocanabinóide; Sistema Imune; Esquizofrenia Fisiopatologia; Neurociências; Sistema endocabinóide
• Link de acesso: http://hdl.handle.net/1843/BUBD-9HDK2M

Schizophrenia is a chronic psychiatric syndrome characterized by generalized cognitive deficits that are responsible for much of the functional impairment associated with the disease. Current treatment options cannot significantly improve cognitive function. Understanding of the pathophysiological mechanisms involved in the cognitive deficits may contribute to the development of better therapeutic strategies. The endocannabinoid system modulates neurotransmission and neuronal plasticity and is important for cognitive functioning. Evidence points to the involvement of this neurotransmitter system in the pathophysiology of schizophrenia and that alteration of the endocannabinoid system in peripheral lymphocytes could reflect central changes. The objective of this study was to find evidence of the involvement of the endocannabinoid system in the pathophysiology of cognitive deficits of schizophrenia. Patients and controls underwent clinical assessment and a cognitive battery (P300 evoked potential, SCoRS and BACS) and the expression of cannabinoid receptors on the surface of peripheral blood lymphocytes and NK cells was assessed by flow cytometry immunophenotyping. The results showed that increase of CB2 receptors on lymphocytes was correlated with impaired cognitive performance in patients. Therefore, the cognitive deficits in schizophrenia may be associated with the expression levels of CB2 receptors on peripheral lymphocytes, and these cells may reflect changes of central cannabinoid receptors in brain areas involved in cognitive processes or in microglial cells, which when activated can contribute to the worsening of cognitive function. These data provide additional evidence of the involvement of the endocannabinoid system in the pathophysiology of cognitive deficits in schizophrenia.