This paper summarizes the plenary and opening talk of WFSBP 2013. In the first half of the talk, three essential messages from cutting - edge biological science to psychiatry (clinical psychiatry) were described as follows: (1) there is one continuum of psychiatric conditions, even beyond the boundary of disease and non - disease; (2) psychiatric conditions are systemic; and (3) psychiatric conditions occur as the results of host- environmental interactions. In the second half of the talk, a short discussion was made on how such biological principles can be applied to clinical psychiatry as effective translation. The significance of acknowledging advantages and limitations of biological science in clinical psychiatry was also emphasized.

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In this symposium, four ketamine researchers summarized their most recent findings. The first speaker, Dr. John Krystal (Department of Psychiatry, Yale University, USA) reported the latest clinical findings of low dose ketamine given alone for its antidepressant actions. Dr. Krystal was the first to describe the use of low dose ketamine in depression. The second speaker, Dr. Nagahisa Okamoto (Sapporo Suzuki Hospital in Sapporo, Japan) presented his research on the advantages of combined ketamine/ECT vs propofol/ECT in therapy- resistant depressed patients. The third speaker, Dr. Hideo Tsukada (Hamamatsu Photonics K.K., Shizuoka, Japan) described his brain PET imaging studies in monkeys that indicate ketamine in low doses is not only an NMDA antagonist but also a serotonin reuptake inhibitor. The latter is a surprising new finding. The fourth speaker, Dr. Edward Domino (Department of Pharmacology, University of Michigan, USA) reviewed the multiple neuropharmacological mechanisms of action of ketamine that account for its antidepressant effects and some of the puzzles this basic research initiated.

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Reward prediction and decision making capacity has been reported to be impaired in various psychiatric disorders. Recently, its brain mechanism has been investigated by sophisticated computational model and neuroimaging studies. Dr. Saori Tanaka, a researcher of neurocomputational model from Osaka University, reviewed the neurocomputational model of reward prediction and decision making. Additionally, she presented her original data about brain mechanism of reward prediction and its change from serotonergic modulation. Professor Damiaan Denys from Department of Psychiatry at University of Amsterdam presented the recent result of an fMRI study that investigated reward prediction in Obsessive Compulsive Disorder (OCD) together with the results from deep brain stimulation in ventral striatum. Lastly, Dr. Yuki Sakai from Department of Psychiatry at Kyoto Prefectural University of Medicine reviewed the studies regarding altered reward prediction and decision making process in psychiatric disorders with serotonergic dysfunction. He focused on OCD, bulimia nervosa and trichotillomania and presented his data from fMRI studies using reward prediction task analyzed by computational model. This symposium was successful in providing a view for mechanistic understanding of altered reward prediction and decision making in some forms of neuropsychiatric disorders by integrating computational model and neuroimaging studies.

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This symposium aims to share knowledge of the importance of investigating brain tissue itself to clarify the pathogenesis of mental illness and how to utilize or/and organize brain banking in the future. The progress in molecular biology facilitated the identification of candidate genes concerning schizophrenia, and most of these genes have a neurodevelopmental function in the CNS. The progress in neuroimaging techniques revealed the morphological brain volume changes of schizophrenia during its course. These studies invigorated neuropathological approaches. We are now on the verge of uncovering the etiology of this disease by integrating cerebral neuroimaging, molecular genetics, and cerebral neuropathology, and its study from the differential approaches might converge with the investigating of brain tissue. In this context, it is important to collect brain tissue and establish the Psychiatric Brain Bank. We have invited two speakers from the Netherlands who have been involved in the Brain Bank from early on. We, the Japanese Society of Biological Psychiatry, are now preparing the Psychiatric Brain Bank in JAPAN, and have much to learn from the pioneers of the brain collection system in EU.

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In patients with schizophrenia, the synchronisation of beta- and gamma- band activity is abnormal, suggesting a crucial role for dysfunctional oscillations in the generation of the cognitive deficits and symptoms of the disorder. Dysfunctional oscillations may arise due to anomalies in the brainʼs rhythm generating networks of γ- aminobutyric acid (GABA) interneurons and deficits in NMDA - receptor functioning. In this symposium, McCarley et al. described findings on optogenetic studies in mice and MRS studies in the schizophrenia spectrum. Uhlhaas et al. presented perspectives for high gamma - band oscillations in schizophrenia and ketamine - induced psychosis in MEG. Tada et al. reported results of electroencephalographic auditory steady state responses (ASSR) in subjects at ultra - high risk and first - episode schizophrenia. Finally, Onitsuka et al. showed MEG - ASSR in patients with schizophrenia and bipolar disorder. Neural oscillations are possible translational paradigms, since they can be recorded from animals, healthy subjects and clinical groups.

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The symposium “Memory manipulation as a therapeutic tool in psychiatry” is organized by Joseph Zophar (Sheba Medical Center, Israel) , who could not join the symposium due to unexpected accidents in his family just before the Congress. There were three speakers in the program; Masatoshi Takeda (Osaka University, Japan) “Early intervention in Alzheimerʼs disease” , Joseph Zohar (Sheba Medical Center, Israel) “Prevention of traumatic memory consolidation as a therapeutic tool in PTSD,” and John Krytal (Yale Iniversity, USA) “Enhancing neuroplasticity with D - cycloserine: Implications for the treatment of anxiety and cognitive disorders.” 　Masatoshi Takeda talked about the mechanism of memory dydfunction in the early stage of Alzheimerʼs disease in which possible involvement of several genes are considered. He pointed out simple stimulation of neurogenesis in the hippocampus will not benefit the dysfunction of the early dementia patients. 　John Krystal talked about the possibility of D- cycloserine treatment to schizophrenia patients, in which D- cycloserine may modulate the hyperactive aberrant neural circuit so that the patients can be ready for incorporating psychotherapeutic intervention.

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Brain - gut peptide hormones are well known modulators of brain functions such as eating and emotional behaviors. Alterations of both central and peripheral peptide signaling have thus been supposed to participate in several psychiatric diseases including eating disorders and depression. The origin of such alteration is often referred as multifactorial but the main common pathophysiological factors have not been determined. Recently, clinical and experimental evidence has emerged supporting a role of plasma immunoglobulins to regulate peptide signaling via direct binding of corresponding peptides. Variability in production and properties of such immunoglobulins or autoantibodies appears to be responsible for the variability of biological effects mediated by corresponding brain - gut peptides. For instance, affinity maturation of a peptide autoantibody was associated with changing of its property from peptide transporting to peptide neutralizing molecule. In the symposium, recent work was presented revealing potential roles of autoantibodies directed against several brain- gut peptide hormones including melanocortin, ACTH, ghrelin and neuropeptide Y in the origin of anorexia nervosa, obesity and depression as well as aggressive behavior. A role of gut inflammation, gut microbiota and nutrition in the regulation of peptide autoantibodies production were also discussed.

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Epilepsy is a risk factor for the development of psychoses, and psychoses could be a risk factor for the development of epilepsy. The continuous bell - curve shape distribution of time interval from onset of epilepsy (psychosis) to that of psychosis (epilepsy) indicates a shared underlying biological mechanism. Brain morphological studies showed widespread grey and white matter changes both in psychoses and epilepsy. Neurodevelopmental deficits may play a role in both psychoses and epilepsy. Recent molecular genetic findings suggest that the comorbidity of psychoses and epilepsy is a product of shared underlying biological mechanisms. A bidirectional relationship between epilepsy and psychoses have been proposed.

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Because SSRI or SNRI has relatively few side effects, they are widely used for treatment of depression as first line. However some new adverse effects of the treatments have been reported. Among them, activation syndrome, rapid cycling, or mixed phase may be prevented by prudent treatments of antidepressants with assessment of bipolarity. So- called new- type depression includes atypical depression which has been confirmed to have biological basis and to need an adjustment of whole monoamines. New SNRI Duloxetine can adjust whole monoamines in the prefrontal cortex. The safety of new SSRI Escitalopram is expected because of its allosteric effect on serotonin transporter.

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Disturbances of cognitive functions, e.g. several types of memory, executive function, attention, verbal fluency, are characteristic of mood disorders and schizophrenia. Imaging techniques in several modalities are likely to provide an objective biomarker for cognitive impairment in these psychiatric illnesses. This issue was discussed interactively in this symposium, based on cutting - edge evidence from near - infrared spectroscopy (presented by Dr. Kazuyuki Nakagome) , functional magnetic resonance imaging (Drs. Steven G. Potkin and Bernardo DellʼOsso) , and positron emission tomography (Dr. Paolo Brambilla) .

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