Clinical Focus

  • Child and Adolescent Psychiatry

Academic Appointments

  • Clinical Assistant Professor, Psychiatry and Behavioral Sciences

Professional Education

  • Board Certification: American Board of Psychiatry and Neurology, Child and Adolescent Psychiatry (2017)
  • Fellowship: Stanford University Child and Adolescent Psychiatry Fellowship (2016) CA
  • Board Certification: American Board of Psychiatry and Neurology, Psychiatry (2015)
  • Residency: University of Pennsylvania Health System (2014) PA
  • Medical Education: University of Virgina School of Medicine (2010) VA

All Publications

  • Asian American Adolescent Help-Seeking Pathways for Psychological Distress ASIAN AMERICAN JOURNAL OF PSYCHOLOGY Chiang, S., Chin, C. A., Meyer, E. W., Sust, S., Chu, J. 2021

    View details for DOI 10.1037/aap0000241

    View details for Web of Science ID 000733195900001

  • The Farewell (Book Review) JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY Book Review Authored by: Thai, J., Sust, S., Kwok, M. 2021; 60 (4): 524–27
  • Integrated Care Assessing and Treating Youth Exposed to Traumatic Stress Grunwald, D., Sust, S. 2019: 429–442
  • Integrated Models ASSESSING AND TREATING YOUTH EXPOSED TO TRAUMATIC STRESS Grunwald, D. S., Sust, S., Carrion, V. G. 2019: 429–42
  • Suicide Among East Asian Youth Suicide Among Diverse Youth Sust, S., Hecht, L., Yu, Z. Springer, Cham. 2017
  • Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models FRONTIERS IN BEHAVIORAL NEUROSCIENCE Choi, C. H., Schoenfeld, B. P., Bell, A. J., Hinchey, J., Rosenfelt, C., Gertner, M. J., Campbell, S. R., Emerson, D., Hinchey, P., Kollaros, M., Ferrick, N. J., Chambers, D. B., Langer, S., Sust, S., Malik, A., Terlizzi, A. M., Liebelt, D. A., Ferreiro, D., Sharma, A., Koenigsberg, E., Choi, R. J., Louneva, N., Arnold, S. E., Featherstone, R. E., Siegel, S. J., Zukin, R., McDonald, T. V., Bolduc, F. V., Jongens, T. A., McBride, S. J. 2016; 10: 136


    Fragile X is the most common monogenic disorder associated with intellectual disability (ID) and autism spectrum disorders (ASD). Additionally, many patients are afflicted with executive dysfunction, ADHD, seizure disorder and sleep disturbances. Fragile X is caused by loss of FMRP expression, which is encoded by the FMR1 gene. Both the fly and mouse models of fragile X are also based on having no functional protein expression of their respective FMR1 homologs. The fly model displays well defined cognitive impairments and structural brain defects and the mouse model, although having subtle behavioral defects, has robust electrophysiological phenotypes and provides a tool to do extensive biochemical analysis of select brain regions. Decreased cAMP signaling has been observed in samples from the fly and mouse models of fragile X as well as in samples derived from human patients. Indeed, we have previously demonstrated that strategies that increase cAMP signaling can rescue short term memory in the fly model and restore DHPG induced mGluR mediated long term depression (LTD) in the hippocampus to proper levels in the mouse model (McBride et al., 2005; Choi et al., 2011, 2015). Here, we demonstrate that the same three strategies used previously with the potential to be used clinically, lithium treatment, PDE-4 inhibitor treatment or mGluR antagonist treatment can rescue long term memory in the fly model and alter the cAMP signaling pathway in the hippocampus of the mouse model.

    View details for DOI 10.3389/fnbeh.2016.00136

    View details for Web of Science ID 000378896600001

    View details for PubMedID 27445731

    View details for PubMedCentralID PMC4928101

  • Epistasis between catechol-O-methyltransferase and type II metabotropic glutamate receptor 3 genes on working memory brain function. Proceedings of the National Academy of Sciences of the United States of America Tan, H. Y., Chen, Q., Sust, S., Buckholtz, J. W., Meyers, J. D., Egan, M. F., Mattay, V. S., Meyer-Lindenberg, A., Weinberger, D. R., Callicott, J. H. 2007; 104 (30): 12536-41


    Dopaminergic and glutamatergic systems are critical components responsible for prefrontal signal-to-noise tuning in working memory. Recent functional MRI (fMRI) studies of genetic variation in these systems in catechol-O-methyltransferase (COMT) and in metabotropic glutamate receptor mgluR3 (GRM3), respectively, suggest that these genes influence prefrontal physiological signal-to-noise in humans. Here, using fMRI, we extend these individual gene findings to examine the combined effects of COMT and GRM3 on dissociable components of the frontoparietal working memory network. We observed an apparent epistatic interaction of these two genes on the engagement of prefrontal cortex during working memory. Specifically, the GRM3 genotype putatively associated with suboptimal glutamatergic signaling was significantly associated with inefficient prefrontal engagement and altered prefrontal-parietal coupling on the background of COMT Val-homozygous genotype. Conversely, COMT Met-homozygous background mediated against the effect of GRM3 genotype. These findings extend putative brain dopaminergic and glutamatergic relationships indexed by COMT and GRM3 to a systems-level interaction in human cortical circuits implicated in working memory dysfunction such as in schizophrenia.

    View details for DOI 10.1073/pnas.0610125104

    View details for PubMedID 17636131

    View details for PubMedCentralID PMC1920538

  • Allelic variation in RGS4 impacts functional and structural connectivity in the human brain. The Journal of neuroscience : the official journal of the Society for Neuroscience Buckholtz, J. W., Meyer-Lindenberg, A., Honea, R. A., Straub, R. E., Pezawas, L., Egan, M. F., Vakkalanka, R., Kolachana, B., Verchinski, B. A., Sust, S., Mattay, V. S., Weinberger, D. R., Callicott, J. H. 2007; 27 (7): 1584-93


    Regulator of G-protein signaling 4 (RGS4) modulates postsynaptic signal transduction by affecting the kinetics of G alpha-GTP binding. Linkage, association, and postmortem studies have implicated the gene encoding RGS4 (RGS4) as a schizophrenia susceptibility factor. Using a multimodal neuroimaging approach, we demonstrate that genetic variation in RGS4 is associated with functional activation and connectivity during working memory in the absence of overt behavioral differences, with regional gray and white matter volume and with gray matter structural connectivity in healthy human subjects. Specifically, variation at one RGS4 single nucleotide polymorphism that has been associated previously with psychosis (rs951436) impacts frontoparietal and frontotemporal blood oxygenation level-dependent response and network coupling during working memory and results in regionally specific reductions in gray and white matter structural volume in individuals carrying the A allele. These findings suggest mechanisms in brain for the association of RGS4 with risk for psychiatric illness.

    View details for DOI 10.1523/JNEUROSCI.5112-06.2007

    View details for PubMedID 17301167

    View details for PubMedCentralID PMC6673752

  • Dysfunctional prefrontal regional specialization and compensation in schizophrenia. The American journal of psychiatry Tan, H. Y., Sust, S., Buckholtz, J. W., Mattay, V. S., Meyer-Lindenberg, A., Egan, M. F., Weinberger, D. R., Callicott, J. H. 2006; 163 (11): 1969-77


    It has been suggested that in healthy persons higher-order cognitive processing engaged by incremental working memory load hierarchically employs more dorsal than ventral prefrontal resources in healthy individuals. Given that working memory performance is impaired in schizophrenia, especially at higher executive loads, the authors investigated how this prefrontal functional organization might be altered in disease, independent of performance deficits.Using N-back working memory functional magnetic resonance imaging (fMRI) data, the authors studied 15 patients with schizophrenia and 26 healthy comparison subjects. Subgroups based on median performance accuracy at 2-back were analyzed; high performers included eight schizophrenia patients and 14 comparison subjects, and low performers included seven patients and 12 comparison subjects.High-performing but not low-performing comparison subjects responded to incremental working memory executive load with disproportionately greater dorsal but not ventral prefrontal cortex activation, which also predicted performance accuracy. In the high- and low-performing patient groups, incremental working memory load caused a disproportionate increase in ventral but not dorsal prefrontal cortex activation relative to the respective comparison group, which also correlated with accuracy. Functional connectivity between the ventral prefrontal cortex and posterior parietal cortex was relatively greater in patients, whereas comparison subjects had greater functional connectivity between the dorsal prefrontal cortex and posterior parietal cortex.The hierarchical organization of the prefrontal cortex may be compromised in schizophrenia, resulting in loss of functional specialization and integration at the dorsal prefrontal cortex and in compensatory activation from the ventral prefrontal cortex, which may ultimately affect working memory and executive cognition.

    View details for DOI 10.1176/ajp.2006.163.11.1969

    View details for PubMedID 17074949