THE ROLE OF FEZI IN COGNITION AND INFERENCES TO MENTAL DISORDERS: A QUALITATIVE ANALYSIS

Abstract

While DISC1 and the dopaminergic hypothesis remain popular in explaining the development of schizophrenia due to dendritic loss and overexpression of dopamine in the CNS, emerging studies have also look at DISC1?s interacting gene, FEZ1. Given that current literature has postulated that FEZ1 helps to promote healthy functioning by facilitating dendritic growth and neurotransmission in the brain, and that the loss of FEZ1 can result in loss of dendritic growth and heightens the risk of schizophrenia, this study aims to investigate the functionality of FEZ1 through localisation techniques that allow for precise examination of FEZ1 within the CNS, and this may contribute to the emerging hypoglutamate hypothesis of schizophrenia. Using rat and monkey CNS tissues, FEZ1 is found to be highly expressed in brain regions with many glutamatergic neurons such as the frontal cortex and hippocampus, as well as the cerebellum, a region of mostly GABAergic neurons. It is also found in abundance within the dendrite of the neurons itself. This implies that FEZ1 is highly involved in not only brain functioning across the brain regions, but also neurotransmission and dendritic growth within the neuron, and loss of FEZ1 may induce hypoglutamatergic state and heighten the risk of schizophrenia.