David Braff, M.D.
Professor of Psychiatry
9500 Gilman Drive
La Jolla, CA 92093-0804C
Phone: (619) 543-5570
FAX: (619) 543-2493
E-mail: dbraff@ucsd.edu

Biography
David Braff, M.D. is Professor of Psychiatry, and Director of the Schizophrenia Program at the University of California, San Diego, School of Medicine.  He is also Director of the NIH-funded Consortium on the Genetics of Schizophrenia (COGS).  He trained at the University of Pennsylvania, Yale University, and the University of California, San Francisco.

Research Focus
David Braff’s research interests have received long-term NIMH and NARSAD funding and a special MERIT Award to extend his research from the NIMH. His research interests center around 1) the identification of inhibitory and information processing deficits in various psychiatric disorders (with an emphasis on schizophrenia); 2) understanding the neural substrate dysfunctions of schizophrenia spectrum subjects using human and translational animal model studies; 3) using information processing deficits, nonlinear (chaos theory) measures, and attentional dysregulation as endophenotypes in family/genetic studies; 4) utilizing translational and genetic research to identify the genetic architecture of neuropsychiatric disorders such as schizophrenia and developing genetically determined, strong inference based targets for developing efficacious antipsychotic medications that can improve the functional outcome and quality of life of schizophrenia patients and reduce the devastating disease burden placed on them and their families by this “no fault” clinical brain disorder.

David Braff has published over 200 articles and 300 reviews, book chapters and abstracts.  He has received special recognition from the ISI as being in the top ½ of 1% of most highly cited psychiatric researchers. In addition, he has treated many patients with schizophrenia and other serious mental disorders. Dr. Braff has served as Vice President and President and is currently the Executive Secretary of the Society of Biological Psychiatry (SOBP). He has served as a Councilor of the American College of Neuropsychopharmacology (ACNP).  He has consulted on the Diagnostic and Statistical Manual, the DSM V Committee, and Expert Treatment Committee of the American Psychiatric Association (APA). He is the Co-Chair of the Executive Committee and Director of the Clinical Neurosciences Unit at the Veterans Administration VISN 22 Mental Illness, Research and Clinical Center (MIRECC) program in the southwest United States investigating psychosis and antipsychotic medications. David Braff has received numerous grants, awards, and prizes. As a Fellow of the APA, Dr. Braff received the Kempf Research Prize, and the Gold Medal for lifetime research accomplishments from the SOBP.  He received the George Thompson Award from the SOBP for service to the field. He has been selected by his peers as one of the “Best Doctors” in the United States and in San Diego. He serves on many national and international committees and societies, such as the Executive Committee of the MATRICS Project of the NIMH, which identified new cognitive targets for new antipsychotic medications, and other NIMH advisory committees that focus on issues such as the design and conduct of large clinical treatment trials.  Dr. Braff is on the Editorial Boards of the Archives of General Psychiatry and five other Journals. He has lectured nationally and internationally on many topics including neuroscience, focusing on schizophrenia and its treatment.

Publications

• DL Braff, MA Geyer. Sensorimotor gating and schizophrenia: Human and animal model studies. Archives of General Psychiatry 47:181-188, 1990.
  Signficance: This paper summarized the neurobiologically-based gating deficits seen in schizophrenia patients and in animal model studies of schizophrenia. The paper established the importance of gating as a key construct in understanding schizophrenia and the utility of animal model studies in studying human psychopathological states.
• DL Braff, R Heaton, M Cullum, I Grant, S Zisook. The generalized pattern of neuropsychological deficits in outpatients with chronic schizophrenia with heterogeneous Wisconsin Card Sorting Test results. Archives of General Psychiatry 48:891-898, 1991.
  Significance: This publication was the first clear description of exactly how widespread neuropsychological deficits (and their corresponding neural substrates) are in schizophrenia.
• W Perry, DL Braff. Information processing deficits and thought disorder in schizophrenia. American Journal of Psychiatry 151:363-367, 1994.
  Significance: One major issue in many studies of prepulse inhibition deficits in schizophrenia patients that had not been resolved was the identification of clinical and functional correlates of these deficits. In this study, we found a significant correlation between prepulse inhibition deficits and thought disorder. In subsequent studies, this correlation increased when prepulse inhibition and thought disorder are measured in close temporal proximity (see #288)
• MP Paulus, N Hozack, B Zauscher, JE McDowell, L Frank, GG Brown, DL Braff. Prefrontal, parietal and temporal cortex networks underlie decision-making in the presence of uncertainty. To appear in NeuroImage.
  Significance: Along with our emerging genetic work in the area of schizophrenia, understanding the neural substrate of information processing deficits is a key goal in the field of schizophrenia research. In this study, the methods applied were derived from non-linear (“chaos”) theory (eg, measures of entropy spectrums) applied to a 2-choice task. We were able to identify the distributed neural network deficiencies that characterize schizophrenia patients.
• DL Braff, R Freedman. The importance of endophenotypes in studies of the genetics of schizophrenia. To appear in, Neuropsychopharmacology: The Fifth Generation of Progress, Lippincott, Williams & Wilkins, Baltimore, MD.
  Significance: This chapter summarizes three decades of work (including many studies conducted in my lab) that have established that 1) information processing deficits occur in schizophrenia patients and their clinically “unaffected” relatives and in schizotypal patients (ie, schizophrenia spectrum non-psychotic patients), 2) many of these markers were developed and refined here at UCSD in my laboratory (eg, visual backward masking, P50 suppression, prepulse inhibition). The markers have a neural circuit basis that has been identified, and 3) the measures can be used as endophenotypes in continuing genetic research in schizophrenia. The ideas in this chapter reflect 30 years of studies using information processing variables, identifying their neural substrates, familial transmission, and segue into a description of how these can be used as endophenotypic markers for schizophrenia, a complex psychiatric genetic disorder.