Glia-neuron interactions as pathophysiological mediators of schizophrenia

Abstract

This thesis focuses on two pivotal facets of the pathophysiology of schizophrenia. Firstly, it examines the impact of glial cell involvement on the disruption of neuronal circuits. Secondly, it elucidates the mechanisms underlying glial cell dysfunction through a comprehensive exploration of the etiology of schizophrenia. Employing a dual approach, it integrates a genetic mutation with microglial cells to uncover the cellular component of inflammation driving cognitive symptoms in schizophrenia. Simultaneously, it investigates how astrocytes serve as conduits for soluble inflammatory markers, studying their influence on the manifestation of positive symptoms in schizophrenia.