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Akira Sawa, M.D. Ph.D.

Molecular and genetic dissection of cognition, emotion, and thought in conjunction with adloescent brain maturation: its application to clinical psychiatry

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University Appointments

Professor of Psychiatry and Behavioral Sciences

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Director, Johns Hopkins Schizophrenia Center
Director, Molecular Psychiatry Program

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Johns Hopkins Schizophrenia Center

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Molecular Psychiatry Program

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Research Interests

The research in our laboratory is directed towards understanding the pathogenesis of major mental illnesses, especially schizophrenia and mood disorders, at the molecular level. Furthermore, we anticipate our efforts may uncover fundamental mechanisms that mediate cognition, emotion, and thought. Taking advantage of our roles in both basic and clinical departments, our approach is interdisciplinary ranging from molecular cellular biology, human genetics, and animal models, to clinical studies using patient subjects. Specifically, we utilize human genetics in two major approaches:

In a top-down approach, we study human subjects with major mental illness and normal controls through multifaceted approaches, which include clinical assessments of psychiatry and psychology, brain imaging (MRI, MRS, and PET), and clinico-electrophysiological means (ERP, EEG, and TMS). In parallel, we conduct molecular dissection of biospecimens from these same sets of subjects. These biospecimens include olfactory neurons obtained through nasal biopsy, induced pluripotent stem cells and induced neurons, and other peripheral cells. In this approach, we evaluate how specific genetic variations affect the phenotypes, which ultimately contribute to disease pathology.

In a bottom-up approach, we focus on concrete molecular targets, such as disease risk gene products and/or key cellular mediators. We identify targets through genetic methods in our patients and in collaboration. Then, we test how these molecular targets are functionally related to each other within cells and neuronal networks of animal models, and how they contribute to disease phenotypes over time, especially in conjunction with adolescent brain maturation. Recently, we are concentrating on neuronal-glial functional interactions.


Niwa, M., Jaaro-Peled, H., Tankou, S., Seshadri, S., Hikida, T., Matsumoto, Y., Cascella, N., Kano, S., Ozaki, N., Nabeshima, T., Sawa, A. (2013). Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids. Science, 339, 335-339.

Kano, S., Colantuoni, C., Han, F., Zhou, Z., Yuan, Q., Wilson, A., Takayanagi, Y., Lee, Y., Rapoport, J., Eaton, W., Cascella, N., Ji, H., Goldman, D., and Sawa, A. (2012). Genome-wide profiling of multiple histone methylations in olfactory cells: further implications for cellular susceptibility to oxidative stress in schizophrenia. Mol Psychiatry, [Epub ahead of print]

Golzio C, Willer J, Talkowski ME, Oh EC, Taniguchi Y, Jacquemont S, Reymond A, Sun M, Sawa A, Gusella JF, Kamiya A, Beckmann JS, Katsanis N. (2012). KCTD13 is a major driver of mirrored neuroanatomical phenotypes of the 16p11.2 copy number variant. Nature 485, 363-367

Ishizuka, K., Kamiya, A., Oh, E.C., Kanki, H., Seshadri, S., Robinson, J.F., Murdoch, H., Dunlop, A.J., Kubo, K., Furukori, K., Huang, B., Zeledon, M., Hayashi-Takagi, A., Okano, H., Nakajima, K., Houslay, M.D., Katsanis, N., and Sawa, A. (2011). DISC1-dependent switch from progenitor proliferation to migration in the developing cortex. Nature 473, 92-96

Brandon, N.J., and Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nat Rev Neurosci 12, 707-722

Kondo, M., and Sawa, A. (2011). Anti-/Propsychotic drug signaling via heteromeric GPCRs--a balancing act? Cell 147, 964-965

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