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Draft:Akira Sawa

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  • 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)

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 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 endowed 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).

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)and also elected to the American Association for the Advancement of Science (AAAS).

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.

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.[4]

The miR-124-AMPAR pathway connectspolygenic risks with behavioral changes shared between schizophrenia and bipolar disorder. Namkung et al, Neuron, 2023, 111:220-235.[5]

Prenatal immune stress blunts microglia reactivity which impairs neurocircuitry. Hayes et al, Nature, 2022, 610:327-324.[6]

A multimodal study of a first episode psychosis cohort: potential markers of antipsychotic treatment resistance. Yang et al, Molecular Psychiatry, 2022, 27:1184-1191.[7]

Improving polygenic prediction in ancestrally diverse populations. Ryan et al, Nature Genetics, 2022, 54:573-580.[8]

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.[9]

The glutathione cycle shapes synaptic glutamate activity. Sedlak et al. Proceedings of the National Academy of Sciences of the USA, 2019, 7:2701-2706.[10]

Aggregation of scaffolding protein DISC1 dysregulates phosphodiesterase 4 in Huntington's disease. Tanaka et al. The Journal Clinical Investigation, 2017,127:1438-1450.[11]

Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids. Niwa et al. Science, 2013, 339:335-339.[12]

DISC1-dependent switch from progenitor proliferation to migration in the developing cortex. Ishizuka et al. Nature, 2011, 473:92-96.[13]

Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1. Hayashi-Takagi et al. Nature Neuroscience, 2010,13:327-332[14]

Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis. Sen et al. Nature Cell Biology, 2008,10:866-873.[15]

S-Nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding. Hara et al. Nature Cell Biology, 2005, 7:665-674. [16]

A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development. Kamiya et al. Nature Cell Biology, 2005,12:1167-78.[17]

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 [18]

The insula: an underestimated brain area in clinical neuroscience, psychiatry, and neurology. Namkung et al. Trends in Neurosciences, 2017, 40:200-207.[19]

Schizophrenia. Owen et al. Lancet, 2016, 388:86-97.[20]

Altering the course of schizophrenia: progress and perspectives. Millan et al. Nature Reviews Drug Discovery, 2016, 15:485-515.[21]

Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Brandon et al. Nature Reviews Neuroscience, 2011,12:707-722.[22]

Schizophrenia: diverse approaches to a complex disease. Sawa et al. Science, 2002, 296:692-695.[23]

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. ^ Prolonged HPA axis dysregulation in postpartum depression associated with adverse early life experiences:a cross-species traslational study.
  5. ^ The miR-124-AMPAR pathway connectspolygenic risks with behavioral changes shared between schizophrenia and bipolar disorder
  6. ^ Prenatal immune stress blunts microglia reactivity which impairs neurocircuitry
  7. ^ A multimodal study of a first episode psychosis cohort: potential markers of antipsychotic treatment resistance
  8. ^ Improving polygenic prediction in ancestrally diverse populations
  9. ^ Assessing brain metabolism with 7-T proton magnetic resonance spectroscopy in patients with first-episode psychosis
  10. ^ The glutathione cycle shapes synaptic glutamate activity
  11. ^ Aggregation of scaffolding protein DISC1 dysregulates phosphodiesterase 4 in Huntington's diseaseT
  12. ^ Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids
  13. ^ DISC1-dependent switch from progenitor proliferation to migration in the developing cortex
  14. ^ Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1
  15. ^ Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis
  16. ^ S-Nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding
  17. ^ A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development
  18. ^ Causal inference on pathophysiological mediators in psychiatry
  19. ^ The insula: an underestimated brain area in clinical neuroscience, psychiatry, and neurology
  20. ^ Schizophrenia
  21. ^ Altering the course of schizophrenia: progress and perspectives
  22. ^ Linking neurodevelopmental and synaptic theories of mental illness through DISC1
  23. ^ Schizophrenia: diverse approaches to a complex disease

Further reading

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  • Johns Hopkins iMIND [1]
  • Johns Hopkins Schizophrenia Center [2]
  • Johns Hopkins School Schizophrenia Center Message from the Director[3]
  • Johns Hopkins University [4]
  • Johns Hopkins Hospital [5]
  • Association of American Physicians（AAP）[6]
  • American Association for the Advancement of Science（AAAS）[7]

Category:Johns Hopkins University faculty Category:University of Tokyo alumni Category:Living people

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