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Draft:Akira Sawa

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  • Comment: Still lacking reliable, independent, secondary sources. Theroadislong (talk) 15:15, 7 August 2024 (UTC)
  • Comment: Currently the submission only uses one source, which is not ideal for verifiability, especially for a biography of a living person such as this submission. Please add additional reliable, independent, secondary sources which provide significant coverage of the subject. Kirbanzo (userpage - talk - contribs) 01:11, 14 April 2020 (UTC)
Akira Sawa
Scientific career
FieldsClinical Psychiatry, Molecular /Cellular Neuroscience, Neuropsychopharmacology
InstitutionsJohns Hopkins UniversityJohns Hopkins Hospital
Doctoral advisorSolomon H. Snyder

Dr. Akira Sawa is a psychiatrist and neuroscientist at Johns Hopkins University and Hospital in Maryland, the United States.

Biography

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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.[1] 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 Innovation Chair of the Johns Hopkins Schizophrenia Center.[2] 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).[3] 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). [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). 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)[5]and also elected to the American Association for the Advancement of Science (AAAS).[6]

Scientific Contributions

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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. His group has conducted multidisciplinary assessments by using longitudinal cohorts for early-stage psychosis and mood disorders. 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. His recent publications exemplify his great versatility and the value of his research contribution.[7][8]

Selected publications (from more than 350 publications）

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Original articles

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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.[9]

The miR-124-AMPAR pathway connectspolygenic risks with behavioral changes shared between schizophrenia and bipolar disorder. Namkung et al, Neuron, 2023, 111:220-235.[10]

Prenatal immune stress blunts microglia reactivity which impairs neurocircuitry. Hayes et al, Nature, 2022, 610:327-324.[11]

A multimodal study of a first episode psychosis cohort: potential markers of antipsychotic treatment resistance. Yang et al, Molecular Psychiatry, 2022, 27:1184-1191.[12]

Improving polygenic prediction in ancestrally diverse populations. Ryan et al, Nature Genetics, 2022, 54:573-580.[13]

Assessing brain metabolism with 7-T proton magnetic resonance spectroscopy in patients with first-episode psychosis. Wang AM et al. JAMA Psychiatry, 2019, 3:314-323.[14]

The glutathione cycle shapes synaptic glutamate activity. Sedlak et al. Proceedings of the National Academy of Sciences of the USA, 2019, 7:2701-2706.[15]

Aggregation of scaffolding protein DISC1 dysregulates phosphodiesterase 4 in Huntington's disease. Tanaka et al. The Journal Clinical Investigation, 2017,127:1438-1450.[16]

Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids. Niwa et al. Science, 2013, 339:335-339.[17]

DISC1-dependent switch from progenitor proliferation to migration in the developing cortex. Ishizuka et al. Nature, 2011, 473:92-96.[18]

Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1. Hayashi-Takagi et al. Nature Neuroscience, 2010,13:327-332[19]

Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis. Sen et al. Nature Cell Biology, 2008,10:866-873.[20]

S-Nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding. Hara et al. Nature Cell Biology, 2005, 7:665-674. [21]

A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development. Kamiya et al. Nature Cell Biology, 2005,12:1167-78.[22]

Review Articles

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Causal inference on pathophysiological mediators in psychiatry. Namkung et al. Cold Spring Harbor Symposia on Quantitative Biology, 2018, 83:17-23 [23]

The insula: an underestimated brain area in clinical neuroscience, psychiatry, and neurology. Namkung et al. Trends in Neurosciences, 2017, 40:200-207.[24]

Schizophrenia. Owen et al. Lancet, 2016, 388:86-97.[25]

Altering the course of schizophrenia: progress and perspectives. Millan et al. Nature Reviews Drug Discovery, 2016, 15:485-515.[26]

Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Brandon et al. Nature Reviews Neuroscience, 2011,12:707-722.[27]

Schizophrenia: diverse approaches to a complex disease. Sawa et al. Science, 2002, 296:692-695.[28]

References

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  1. ^ "Akira Sawa MD, PHD Professor of Psychiatry and Behavioral Sciences", neuroscience.jhu.edu, retrieved July 20, 2024
  2. ^ The Schizophrenia Center Message from the Dorector, retrieved July 20, 2024
  3. ^ iMIND, retrieved July 20, 2024
  4. ^ Akira Sawa's profile
  5. ^ Directory of AAP
  6. ^ AAAS Fellows 2023
  7. ^ Akira Sawa's full list of publications
  8. ^ patents
  9. ^ 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, PMID 38736646
  10. ^ Namkung, H.; Yukitake, H.; Fukudome, D.; Lee, B. J.; Tian, M.; Ursini, G.; Saito, A.; Lam, S.; Kannan, S.; Srivastava, R.; Niwa, M.; Sharma, K.; Zandi, P.; Jaaro-Peled, H.; Ishizuka, K.; Chatterjee, N.; Huganir, R. L.; Sawa, A. (2023), "The miR-124-AMPAR pathway connectspolygenic risks with behavioral changes shared between schizophrenia and bipolar disorder", Neuron, 111 (2): 220–235.e9, doi:10.1016/j.neuron.2022.10.031, PMC 10183200, PMID 36379214
  11. ^ 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, doi:10.1038/s41586-022-05274-z, PMID 36171283
  12. ^ 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, PMID 34642460
  13. ^ 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, PMID 35513724
  14. ^ Wang, A. M.; Pradhan, S.; Coughlin, J. M.; Trivedi, A.; Dubois, S. L.; Crawford, J. L.; Sedlak, T. W.; Nucifora Jr, F. C.; Nestadt, G.; Nucifora, L. G.; Schretlen, D. J.; Sawa, A.; Barker, P. B. (2019), "Assessing brain metabolism with 7-T proton magnetic resonance spectroscopy in patients with first-episode psychosis", JAMA Psychiatry, 76 (3): 314–323, doi:10.1001/jamapsychiatry.2018.3637, PMC 6439827, PMID 30624573
  15. ^ Sedlak, T. W.; Paul, B. D.; Parker, G. M.; Hester, L. D.; Snowman, A. M.; Taniguchi, Y.; Kamiya, A.; Snyder, S. H.; Sawa, A. (2019), "The glutathione cycle shapes synaptic glutamate activity", Proceedings of the National Academy of Sciences of the United States of America, 116 (7): 2701–2706, Bibcode:2019PNAS..116.2701S, doi:10.1073/pnas.1817885116, PMC 6377501, PMID 30692251
  16. ^ Tanaka, M.; Ishizuka, K.; Nekooki-Machida, Y.; Endo, R.; Takashima, N.; Sasaki, H.; Komi, Y.; Gathercole, A.; Huston, E.; Ishii, K.; Hui, K. K.; Kurosawa, M.; Kim, S. H.; Nukina, N.; Takimoto, E.; Houslay, M. D.; Sawa, A. (2017), "Aggregation of scaffolding protein DISC1 dysregulates phosphodiesterase 4 in Huntington's diseaseT", The Journal of Clinical Investigation, 127 (4): 1438–1450, doi:10.1172/JCI85594, PMC 5373889, PMID 28263187
  17. ^ 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
  18. ^ 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
  19. ^ Hayashi-Takagi, A.; Takaki, M.; Graziane, N.; Seshadri, S.; Murdoch, H.; Dunlop, A. J.; Makino, Y.; Seshadri, A. J.; Ishizuka, K.; Srivastava, D. P.; Xie, Z.; Baraban, J. M.; Houslay, M. D.; Tomoda, T.; Brandon, N. J.; Kamiya, A.; Yan, Z.; Penzes, P.; Sawa, A. (2010), "Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1", Nature Neuroscience, 13 (3): 327–332, doi:10.1038/nn.2487, PMC 2846623, PMID 20139976
  20. ^ Sen, N.; Hara, M. R.; Kornberg, M. D.; Cascio, M. B.; Bae, B. I.; Shahani, N.; Thomas, B.; Dawson, T. M.; Dawson, V. L.; Snyder, S. H.; Sawa, A. (2008), "Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis", Nature Cell Biology, 10 (7): 866–873, doi:10.1038/ncb1747, PMC 2689382, PMID 18552833
  21. ^ Hara, M. R.; Agrawal, N.; Kim, S. F.; Cascio, M. B.; Fujimuro, M.; Ozeki, Y.; Takahashi, M.; Cheah, J. H.; Tankou, S. K.; Hester, L. D.; Ferris, C. D.; Hayward, S. D.; Snyder, S. H.; Sawa, A. (2005), "S-Nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding", Nature Cell Biology, 7 (7): 665–674, doi:10.1038/ncb1268, PMID 15951807
  22. ^ Kamiya, A.; Kubo, K.; Tomoda, T.; Takaki, M.; Youn, R.; Ozeki, Y.; Sawamura, N.; Park, U.; Kudo, C.; Okawa, M.; Ross, C. A.; Hatten, M. E.; Nakajima, K.; Sawa, A. (2005), "A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development", Nature Cell Biology, 7 (12): 1167–1178, doi:10.1038/ncb1328, PMID 16299498
  23. ^ Namkung, H.; Lee, B. J.; Sawa, A. (2018), "Causal inference on pathophysiological mediators in psychiatry", Cold Spring Harbor Symposia on Quantitative Biology, 83: 17–23, doi:10.1101/sqb.2018.83.037655, PMID 30850434
  24. ^ Namkung, H.; Kim, S. H.; Sawa, A. (2017), "The insula: an underestimated brain area in clinical neuroscience, psychiatry, and neurology", Trends in Neurosciences, 40 (4): 200–207, doi:10.1016/j.tins.2017.02.002, PMC 5538352, PMID 28314446
  25. ^ Owen, M. J.; Sawa, A.; Mortensen, P. B. (2016), "Schizophrenia", Lancet (London, England), 388 (10039): 86–97, doi:10.1016/S0140-6736(15)01121-6, PMC 4940219, PMID 26777917
  26. ^ Millan, M. J.; Andrieux, A.; Bartzokis, G.; Cadenhead, K.; Dazzan, P.; Fusar-Poli, P.; Gallinat, J.; Giedd, J.; Grayson, D. R.; Heinrichs, M.; Kahn, R.; Krebs, M. O.; Leboyer, M.; Lewis, D.; Marin, O.; Marin, P.; Meyer-Lindenberg, A.; McGorry, P.; McGuire, P.; Owen, M. J.; Patterson, P.; Sawa, A.; Spedding, M.; Uhlhaas, P.; Vaccarino, F.; Wahlestedt, C.; Weinberger, D. (2016), "Altering the course of schizophrenia: progress and perspectives", Nature Reviews. Drug Discovery, 15 (7): 485–515, doi:10.1038/nrd.2016.28, PMID 26939910
  27. ^ 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
  28. ^ Sawa, A.; Snyder, S. H. (2002), "Schizophrenia: diverse approaches to a complex disease", Science, 296 (5568): 692–695, Bibcode:2002Sci...296..692S, doi:10.1126/science.1070532, PMID 11976442

Further reading

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  • 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]

Category:Johns Hopkins University faculty Category:American medical researchers Category:American psychiatrists Category:American neuroscientists Category:Johns Hopkins School of Medicine alumni Category:Fellows of the American Association for the Advancement of Science Category:Living peopleq

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