Akira Sawa
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Dr. Akira Sawa is a psychiatrist and neuroscientist at Johns Hopkins University and Hospital in Maryland, the United States.
Biography
Dr.Sawa graduated from the University of Tokyo and received his M.D. degree in 1990. He initially completed clinical training in psychiatry and research training in molecular neuroscience under Dr. Solomon H. Snyder at Johns Hopkins University. Dr. Sawa then started his career as an independent faculty investigator at Johns Hopkins University and Hospital in 2002. Since 2012, he has served as the director and endowed chair of the Johns Hopkins Schizophrenia Center[1]. The center focuses on patient care, research, education, and public outreach for psychotic disorders, such as schizophrenia.. In 2020, Dr. Sawa started to lead a multi-disciplinary and multi-departmental initiative named Johns Hopkins iMIND (Institute for Mental Innovation and NeuroDiscovery).[2] Based on Dr. Sawa’s training in both clinical psychiatry and basic molecular neuroscience, he leads Johns Hopkins iMIND to address mechanistic questions for major mental illnesses, such as schizophrenia, mood disorders, and Alzheimer’s disease, with a particular emphasis on early detection and early intervention of these conditions. Dr. Sawa belongs to 6 departments among 2 schools within the Johns Hopkins University as a professor (psychiatry, neuroscience, biomedical engineering, genetic medicine, and pharmacology at the School of Medicine and mental health at the Bloomberg School of Public Health).[3][4]
Dr.Sawa belongs to multiple academic societies and charities as a Fellow, Council member, and Committee member, including the American Psychiatric Association(APA), the Society for Neuroscience(SFN), the American College of Neuropsychopharmacology(ACNP), the Schizophrenia International Research Society(SIRS), and the Brain & Behavior Research Foundation(BBRF)[5]. Dr. Sawa also contributes to global scientific agencies and centers as an advisory member, such as those of the Medical Research Council (MRC) and Wellcome Trust in the UK. Dr. Sawa was elected to the Association of American Physicians (AAP)[6] and also elected to the American Association for the Advancement of Science (AAAS)[7]
Scientific Contributions
Based on Dr. Sawa’s training in both clinical psychiatry and basic molecular neuroscience, the research program that he is organizing aims towards multidisciplinary, translational studies for major mental illnesses, such as schizophrenia, mood disorders (bipolar disorder and major depressive disorder), and Alzheimer’s disease, with a particular emphasis on early detection and early intervention of these conditions. This research pays attention to genetic factors, environmental stressors, and the interaction of gene-environmental factors in the disease trajectory.[8],[9],[10],[11],[12],[13],[14] His group has conducted multidisciplinary assessments by using longitudinal cohorts for early-stage psychosis and mood disorders.[8],[15],[9],[16],[17] As a result, his group has identified several critical biological and molecular changes associated with the disease condition, particularly reporting the disturbance of molecules in homeostatic signaling, redox, and immune/inflammatory responses. Brain imaging data available in the same cohorts have provided further insight on how the alteration of homeostatic signaling cascades contributes to the neurocircuitry alteration and clinical manifestations. By using rodent models, his group has demonstrated and proven several mechanisms that can underlie molecular/brain imaging features in the disease condition under the light of developmental trajectory.[8],[9],[12] His recent publications exemplify his great versatility and the value of his research contribution.[18],[19]
Selected publications (from more than 350 publications）
Prolonged HPA axis dysregulation in postpartum depression associated with adverse early life experiences: a cross-species translational study. Niwa et al. Nature Mental Health, 2024, 2:594-604.[20]
The miR-124-AMPAR pathway connectspolygenic risks with behavioral changes shared between schizophrenia and bipolar disorder. Namkung et al., Neuron, 2023, 111:220-235.[21]
Prenatal immune stress blunts microglia reactivity which impairs neurocircuitry. Hayes et al., Nature, 2022, 610:327-324.[22]
A multimodal study of a first episode psychosis cohort: potential markers of antipsychotic treatment resistance. Yang et al., Molecular Psychiatry, 2022, 27:1184-1191.[23]
Improving polygenic prediction in ancestrally diverse populations. Ryan et al., Nature Genetics, 2022, 54:573-580.[24]
Molecular substrates of schizophrenia: homeostatic signaling to connectivity. Landek-Salgado et al, Molecular Psychiatry, 2016, 21:1:10-28 https://pubmed.ncbi.nlm.nih.gov/26390828/
Schizophrenia. Owen et al. Lancet, 2016, 388:86-97.[25]
Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids. Niwa et al. Science, 2013, 339:335-339.[26]
Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Brandon et al. Nature Reviews Neuroscience, 2011,12:707-722.[27]
DISC1-dependent switch from progenitor proliferation to migration in the developing cortex. Ishizuka et al, Nature, 2011,473:92-96 [28]
References
- ↑ Johns Hopkins Schizophrenia Center
- ↑ iMIND
- ↑ Akira Sawa's profile at Johns Hopkins Medicine
- ↑ Akira Sawa's profile at Johns Hopkins Blloming School of Public Health
- ↑ Brain & Behavior Research Foundation, 20 April 2017
- ↑ Association of American Physicians
- ↑ American Association for the Advancement of Science
- ↑ 8.0 8.1 8.2 Niwa, M.; Lockhart, S.; Wood, D. J.; Yang, K.; Francis-Oliveira, J.; Kin, K.; Ahmed, A.; Wand, G. S.; Kano, S. I.; Payne, J. L.; Sawa, A. (2024), "Prolonged HPA axis dysregulation in postpartum depression associated with adverse early life experiences: A cross-species translational study", Nature. Mental Health, 2 (5): 593–604, doi:10.1038/s44220-024-00217-1, PMC 11087073 Check
|pmc=value (help), PMID 38736646 Check|pmid=value (help) - ↑ 9.0 9.1 9.2 Hayes, L. N.; An, K.; Carloni, E.; Li, F.; Vincent, E.; Trippaers, C.; Paranjpe, M.; Dölen, G.; Goff, L. A.; Ramos, A.; Kano, S. I.; Sawa, A. (2022), "Prenatal immune stress blunts microglia reactivity, impairing neurocircuitry", Nature, 610 (7931): 327–334, Bibcode:2022Natur.610..327H, doi:10.1038/s41586-022-05274-z, PMID 36171283 Check
|pmid=value (help) - ↑ Landek-Salgado, M. A.; Faust, T. E.; Sawa, A. (2016), "Molecular substrates of schizophrenia: Homeostatic signaling to connectivity", Molecular Psychiatry, 21 (1): 10–28, doi:10.1038/mp.2015.141, PMC 4684728, PMID 26390828
- ↑ Owen, Michael J; Sawa, Akira; Mortensen, Preben B (July 2016). "Schizophrenia". The Lancet. 388 (10039): 86–97. doi:10.1016/S0140-6736(15)01121-6.
- ↑ 12.0 12.1 Niwa, M.; Jaaro-Peled, H.; Tankou, S.; Seshadri, S.; Hikida, T.; Matsumoto, Y.; Cascella, N. G.; Kano, S.; Ozaki, N.; Nabeshima, T.; Sawa, A. (2013), "Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids", Science, 339 (6117): 335–339, Bibcode:2013Sci...339..335N, doi:10.1126/science.1226931, PMC 3617477, PMID 23329051
- ↑ Brandon, N. J.; Sawa, A. (2011), "Linking neurodevelopmental and synaptic theories of mental illness through DISC1", Nature Reviews. Neuroscience, 12 (12): 707–722, doi:10.1038/nrn3120, PMC 3954824, PMID 22095064
- ↑ 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.; Sawa, A. (2011), "DISC1-dependent switch from progenitor proliferation to migration in the developing cortex", Nature, 473 (7345): 92–96, Bibcode:2011Natur.473...92I, doi:10.1038/nature09859, PMC 3088774, PMID 21471969
- ↑ Yang, K.; Longo, L.; Narita, Z.; Cascella, N.; Nucifora Jr, F. C.; Coughlin, J. M.; Nestadt, G.; Sedlak, T. W.; Mihaljevic, M.; Wang, M.; Kenkare, A.; Nagpal, A.; Sethi, M.; Kelly, A.; Di Carlo, P.; Kamath, V.; Faria, A.; Barker, P.; Sawa, A. (2022), "A multimodal study of a first episode psychosis cohort: Potential markers of antipsychotic treatment resistance", Molecular Psychiatry, 27 (2): 1184–1191, doi:10.1038/s41380-021-01331-7, PMC 9001745 Check
|pmc=value (help), PMID 34642460 Check|pmid=value (help) - ↑ Ruan, Y.; Lin, Y. F.; Feng, Y. A.; Chen, C. Y.; Lam, M.; Guo, Z.; Stanley Global Asia, Initiatives; He, L.; Sawa, A.; Martin, A. R.; Qin, S.; Huang, H.; Ge, T. (2022), "Improving polygenic prediction in ancestrally diverse populations", Nature Genetics, 54 (5): 573–580, doi:10.1038/s41588-022-01054-7, PMC 9117455 Check
|pmc=value (help), PMID 35513724 Check|pmid=value (help) - ↑ 18.0 18.1 My Bibliography - NCBI
- ↑ Google Patents
- ↑ Niwa, M.; Lockhart, S.; Wood, D. J.; Yang, K.; Francis-Oliveira, J.; Kin, K.; Ahmed, A.; Wand, G. S.; Kano, S. I.; Payne, J. L.; Sawa, A. (2024), "Prolonged HPA axis dysregulation in postpartum depression associated with adverse early life experiences:a cross-species traslational study.", Nature. Mental Health, 2 (5): 593–604, doi:10.1038/s44220-024-00217-1, PMC 11087073 Check
|pmc=value (help), PMID 38736646 Check|pmid=value (help) - ↑ Hayes, L. N.; An, K.; Carloni, E.; Li, F.; Vincent, E.; Trippaers, C.; Paranjpe, M.; Dölen, G.; Goff, L. A.; Ramos, A.; Kano, S. I.; Sawa, A. (2022), "Prenatal immune stress blunts microglia reactivity which impairs neurocircuitry", Nature, 610 (7931): 327–334, Bibcode:2022Natur.610..327H, doi:10.1038/s41586-022-05274-z, PMID 36171283 Check
|pmid=value (help) - ↑ Yang, K.; Longo, L.; Narita, Z.; Cascella, N.; Nucifora Jr, F. C.; Coughlin, J. M.; Nestadt, G.; Sedlak, T. W.; Mihaljevic, M.; Wang, M.; Kenkare, A.; Nagpal, A.; Sethi, M.; Kelly, A.; Di Carlo, P.; Kamath, V.; Faria, A.; Barker, P.; Sawa, A. (2022), "A multimodal study of a first episode psychosis cohort: potential markers of antipsychotic treatment resistance", Molecular Psychiatry, 27 (2): 1184–1191, doi:10.1038/s41380-021-01331-7, PMC 9001745 Check
|pmc=value (help), PMID 34642460 Check|pmid=value (help) - ↑ Ruan, Y.; Lin, Y. F.; Feng, Y. A.; Chen, C. Y.; Lam, M.; Guo, Z.; Stanley Global Asia, Initiatives; He, L.; Sawa, A.; Martin, A. R.; Qin, S.; Huang, H.; Ge, T. (2022), "Improving polygenic prediction in ancestrally diverse populations", Nature Genetics, 54 (5): 573–580, doi:10.1038/s41588-022-01054-7, PMC 9117455 Check
|pmc=value (help), PMID 35513724 Check|pmid=value (help) - ↑ Owen, M. J.; Sawa, A.; Mortensen, P. B. (2016), "Schizophrenia", Lancet, 388 (10039): 86–97, doi:10.1016/S0140-6736(15)01121-6, PMC 4940219, PMID 26777917
- ↑ Niwa, M.; Jaaro-Peled, H.; Tankou, S.; Seshadri, S.; Hikida, T.; Matsumoto, Y.; Cascella, N. G.; Kano, S.; Ozaki, N.; Nabeshima, T.; Sawa, A. (2013), "Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids", Science, 339 (6117): 335–339, Bibcode:2013Sci...339..335N, doi:10.1126/science.1226931, PMC 3617477, PMID 23329051
- ↑ Brandon, N. J.; Sawa, A. (2011), "Linking neurodevelopmental and synaptic theories of mental illness through DISC1", Nature Reviews. Neuroscience, 12 (12): 707–722, doi:10.1038/nrn3120, PMC 3954824, PMID 22095064
- ↑ 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.; Sawa, A. (2011). "DISC1-dependent switch from progenitor proliferation to migration in the developing cortex". Nature. 473 (7345): 92–96. Bibcode:2011Natur.473...92I. doi:10.1038/nature09859. PMC 3088774. PMID 21471969.
Further reading
- Johns Hopkins iMIND [1][2]
- Johns Hopkins Schizophrenia Center [3]
- Johns Hopkins School Schizophrenia Center Message from the Director[4]
- Johns Hopkins University [5]
- Johns Hopkins Hospital [6]
- Association of American Physicians（AAP）[7]
- American Association for the Advancement of Science（AAAS）[8]
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