Akira Sawa, Johns Hopkins University Hospital, USA

Akira Sawa

Akira Sawa, M.D. is a psychiatrist and neuroscientist at the Johns Hopkins University and Hospital in Baltimore, (USA). His research combines clinical-based studies with experimental lab work to understand molecular, cellular, and circuitry mechanisms that underlie cognition, emotional control, and social function.

Sawa moved to the USA in the early stages of his professional career for further training in neuroscience and psychiatry after his initial education in clinical psychiatry in Japan. Sawa started his career as an independent faculty investigator at Johns Hopkins University and Hospital in 2002. Since 2012, Sawa serves as the Director and Endowed Chair of the Johns Hopkins Schizophrenia Center, that is in charge of patient care, research, education, and public outreach for psychotic disorders and severe mental disorders. The Center functions as a hub of multi-departmental research coalitions for these disorders. Sawa is also a Professor of Psychiatry, Mental Health, Neuroscience, and Biomedical Engineering at Johns Hopkins University School of Medicine, Johns Hopkins Bloomberg School of Public Health, and Johns Hopkins Hospital.

Sawa belongs to multiple academic societies and charities as a Fellow, Council member, or Committee member, including the American Psychiatric Association (APA), the Society for Neuroscience (SFN), the Schizophrenia International Research Society (SIRS), the American College of Neuropsychopharmacology (ACNP), and the Brain Behavior Research Foundation (BBRF). Sawa also contributes to global scientific agencies, such as the Medical Research Council (MRC) and the Wellcome Trust in the UK, as an advisory member.

Presentation abstract

Molecular and imaging biomarkers of first episode psychosis: novel cytokine and chemokine signalling pathways

Professor Akira Sawa, M.D.
Johns Hopkins Schizophrenia Center
Departments of Psychiatry, Mental Health, Neuroscience, and Biomedical Engineering
Johns Hopkins University School of Medicine and Bloomberg School of Public Health
600 N. Wolfe Street, Baltimore MD 21287
Email addresses are provided for information in connection with the authors presentation only. Please do not mail credit card information under any circumstances.

Studies have provided a comprehensive landscape of the genetic architecture that underlies major mental illness. These findings can support hypotheses for pathways in the pathophysiology underlying the multi-factorial pathogenesis of psychiatric diseases. Nevertheless, most of these genetic discoveries do not have direct clinical application yet. Thus, it is important to investigate the key mediators in pathophysiology that serve as convergent outcomes of multiple genetic and environmental factors.

The notion of interfering with key biological processes before the full chronic expression of disease symptoms has many precedents, including those in cardiovascular disease and diabetes. Likewise, many researchers have begun to pay more attention to first episode psychosis in the study of schizophrenia (SZ) and mood disorders.

We have conducted both hypothesis-driven and unbiased (hypothesis-free) analyses to look for molecular signatures that are associated with specific symptoms underlying these major mental illnesses. For this, we recruit patients with first episode psychosis and those with chronic schizophrenia, as well as matched healthy controls. Our study includes multifaceted assessments that contain multiple tissue biopsies and cells, brain imaging, and clinical evaluation.

In the present study, we found that a set of cytokines and chemokines are aberrantly expressed in patients with psychosis. They also displayed an alteration in neural circuitry detected by resting-state functional MRI. To address the mechanisms that link these molecular changes specific to circuitry and behavioural alterations, we used a drug-induced mouse model that displays psychostimulant hypersensitivity in which we observed primary changes in the cytokine/chemokine signalling pathway in the hippocampus and the resultant neurocircuitry alteration in the prefrontal cortex. Blockade of this circuitry disturbance ameliorated the behavioural deficits.

Together, by utilizing both human and animal studies, we propose novel cytokine and chemokine signalling pathways in the hippocampal/prefrontal circuits as a driver of psychotic symptoms. 

Funding: NIH, S-R foundation, NARSAD, Stanley

Conflicts of interest: A part of study participants’ recruitment was funded by the Mitsubishi Tanabe Pharm. Co. Ltd.


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Supporting Publications
Organised by
  • Elsevier
  • TLP
  • TLN
  • Autoimmune Encephalitis (AE) Alliance
  • Encephalitis Society
  • Treating Autism