Ruben Gur

Professor of Psychology, Radiology and Neurology and Director of the Brain Behavior Laboratory in the University of Pennsylvania Psychiatry Department.
Dr. Gur received his B.A. in Psychology and Philosophy from the Hebrew University of Jerusalem, Israel, in 1970 and his M.A. and Ph.D. in Psychology (Clinical) from Michigan State University in 1971 and 1973, respectively. He did Postdoctoral training with E.R. Hilgard at Stanford University and came to Penn as Assistant Professor in 1974. His research has been in the study of brain and behavior in healthy people and patients with brain disorders, with a special emphasis on exploiting neuroimaging as experimental probes. His work has documented sex differences, aging effects, and abnormalities in regional brain function associated with schizophrenia, affective disorders, stroke, epilepsy, movement disorders and dementia. His work has been supported by grants from the NSF, NIH, NIMH, NIA, NINDS, private foundations (Spencer, MacArthur, EJLB) and industry (BioLogic, Novo, Pfizer).
Multimodal brain and behavior indices of psychosis risk

With the increased emphasis on mechanistic accounts of psychosis that can lead to early detection and intervention, early indicators of psychosis risk can provide the tools for theoretical understanding that can inform treatment. Most studies have used clinical manifestations of subthreshold symptoms in help-seeking individuals to target samples for followup. The Philadelphia neurodevelopmental Cohort uniquely provides a community-based sample with clinical and neurocognitive data on about 9,500 youths and multimodal neuroimaging data on a subsample of about 1,600. Followup data at about 2 years were obtained, including neuroimaging, on a sample of 500 youths, of whom about half had reported psychotic symptoms at intake and the rest reported no psychiatric symptoms.
We present data from the intake evaluation, showing that individuals who report psychotic symptoms have neurocognitive deficits and delayed development of neurocognitive performance landmarks. These deficits were most pronounced for executive functions and social cognition but were also significant for memory and complex cognition. Predictors of maintaining high-risk status for psychosis were more specific. They had worse neurocognitive performance at intake for face memory and social cognition. For the subsample with neuroimaging data at intake, the best predictors of continued psychotic symptoms were brain volumes, which were lower for striatal, limbic and cortical regions also implicated in adults with psychosis.
It appears that the combination of clinical and brain-behavior data can provide a powerful set of predictors of persistence of psychotic symptoms. These measures can also provide mechanistic insights, especially when linked with genomic data, and suggest avenues for intervention by delineating vulnerable brain systems linked to circumscribed neurocognitive domains.