Invited Speaker

Phospholipids Turnover and Arachidonate Signaling in Schizophrenia
Jeffrey K. Yao, Erik Messamore
USA

Schizophrenia is a remarkably complex disorder with a multitude of behavioral and biological perturbations. Whether these diverse alterations are independent biological processes or a result of a more fundamental pathology has yet to be determined. Phospholipid hypotheses of schizophrenia etiology are compelling because they can explain many of the seemingly disparate alterations reported in schizophrenia. Over the years, we have discovered many leads regarding schizophrenia-associated abnormalities in membrane phospholipids, polyunsaturated fatty acids, oxidative stress, and monoamine metabolites. Conceptually, these defects can all be linked together with arachidonic acid (AA) as a nexus point in the cascade leading to the syndrome of schizophrenia, representing a common biochemical pathway leading to the highly heterogeneous symptomatology of psychosis. The primary goal of this investigation is to assess the physiological consequence of altered AA signaling and how they relate to the neurobiological manifestations of schizophrenia. Since no currently used medications specifically address any aspect of phospholipid metabolism or AA signaling, the information to be gained from our study will provide novel windows of therapeutic opportunity. Further, if AA signaling abnormalities represent a physiologically distinct endophenotype within the complex schizophrenia syndrome, our findings could open new avenues in personalized medicine for this patient population.