Fri. Oct 11, 2019 8:40 AM - 10:20 AM Room 15 (Palace Room B)

Organizer / Chair: Hiroyuki UCHIDA (Department of Neuropsychiatry, Keio University School of Medicine, Japan), Co-chair: Makoto HIGUCHI (Department of Functional Brain Imaging Research, National Institute of Radiological Sciences, Japan), Discussants: ‌Yuan-Hwa CHOU (Taipei Veterans General Hospital, Taiwan), Mitsuyuki MATSUMOTO (Virtual Venture Unit, Psychiatry, Astellas Research Institute of America, San Diego, USA)

Advances in research of psychopharmacology have brought the hope for the treatment of psychiatric disorders. With the development of brain image techniques clinicians can learn more detailed information from the brain of psychiatric patients and devise more effective treatment strategies for them. The purpose of this symposium is to provide the state-of-art knowledge on treatment response, cognitions, and pathophysiology of the psychiatric illnesses that have been discovered with brain imaging. This symposium will provide the knowledge on, not only brain imaging itself, but also its application to clinical practice as well as research.
The first speaker will discuss predictors of antipsychotic responsiveness in first episode psychosis (FEP). It has been reported that dopaminergic activity in schizophrenia is related to responsiveness to antipsychotic drugs. For example, patients who respond well to first-line antipsychotic drugs show increased presynaptic dopamine synthesis, while treatment-refractory patients with schizophrenia exhibited a similar level of dopamine activity. The refractory schizophrenia is considered to be related with glutamatergic abnormality. Regarding antipsychotic responsiveness, different neurobiology may underlie schizophrenia between treatment responsive and treatment refractory patients. In this presentation, the speaker will review the evidence on presynaptic dopamine activity and glutamate level measured in drug-naïve FEP and their relationship with antipsychotic responsiveness.
The topic from second speaker will be “Neurobiology of cognitive deficits and treatment implications”. The evidence from several lines of research suggests the differential neurobiology for positive and cognitive symptoms of schizophrenia; while decreased dopamine release is considered to underlie the neurocognitive symptoms, neuropeptides play a critical role in the pathogenesis of social cognitive deficits typically seen in schizophrenia. This difference in neurobiology makes a strong case for rational use of add on interventions for the treatment of cognitive deficits in schizophrenia. Psychostimulants in the form of dopamine agonists and neuropeptides oxytocin - vasopressin are potential novel treatments for cognitive deficits in schizophrenia. This talk will focus on the neuroimaging studies examining the neurobiology of cognitive deficits and potential treatment for the same.
The third speaker will show the recent data on AMPA receptors (AMPAR) in multiple psychiatric illnesses. With the development of a new ligand, we can visualize AMPAR in the living human brain. The results from our pilot study have already revealed distinct patterns of AMPAR distributions in major psychiatric illnesses, including schizophrenia. Clinical relevance of these findings will also be discussed.
The last speaker will present “glutamatergic dysfunction in treatment-resistant schizophrenia: a 3T proton MRS study”. In terms of antipsychotic treatment response, patients with schizophrenia can be classified into three groups: (1) responsive to first-line antipsychotics (non treatment-resistant schizophrenia [nTRS]), (2) treatment-resistant to non-clozapine (CLZ) antipsychotics but CLZ-responsive (non-URS), and (3) treatment-resistant to both non-CLZ antipsychotics as well as CLZ (ultra treatment-resistant schizophrenia [URS]). The glutamatergic hypothesis may account for this classification. Thus, the aim of this presentation is to systematically review proton magnetic resonance spectroscopy (1H-MRS) studies to compare glutamatergic neurometabolite levels among these three patient groups and healthy controls (HCs).