Jennifer Forsyth

Image of Jennifer Forsyth

Jennifer Forsyth, Ph.D.

Assistant Professor
Kincaid 527B
Advising: Possibly accepting new graduate students in 2023-2024, please email with questions.
Interests: Genetic, neurobiological, and environmental mechanisms underlying schizophrenia and related disorders, brain development


The emergence of psychotic symptoms and related impairments in adolescence or early adulthood associated with schizophrenia can be devastating for patients and their families. Understanding why these symptoms emerge for some individuals and not others, with the long-term aim to improve our ability to alter illness trajectory or even prevent psychotic symptom onset, is the primary focus of my research. I am particularly interested in understanding the pathways from genes to neural- and systems-level dysfunction in psychotic disorders, including understanding how variability in genetic factors contributes to variability in clinical presentation among patients. I am also interested in understanding how genetic and environmental factors shape broader psychiatric and related phenotypes, including understanding how specific genetic variants, such as known, pathogenic copy number variants, contribute to risk for multiple psychiatric disorders. To pursue these questions, my lab incorporates genetic, neuroimaging (i.e., MRI and EEG), and behavioral methods.

Representative Publications:
Forsyth, J. K., Mennigen, E., Lin, A., Sun, D., Vajda, A., Kushan-Wells, L., Ching, C. R. K., Villalon-Reina, J. E., 22q11.2 ENIGMA Consortium, Thompson, P. M., Bearden, C. E. Prioritizing Genetic Contributors to Cortical Alterations in 22q11.2 Deletion Syndrome Using Imaging Transcriptomics. (2021). Cerebral Cortex, 31(7), 3285-3298.

Forsyth, J. K., Nachun, D., Gandal, M. J., Geschwind, G., Anderson, A. E., Coppola, G., Bearden, C. E. (2020). Synaptic and gene regulatory mechanisms in schizophrenia, autism, and 22q11.2 copy number variant-mediated risk for neuropsychiatric disorders. Biological Psychiatry, 87(2), 150-163.

Cao H, Chen OY, Chung Y, Forsyth JK, McEwen S, Gee DG, Bearden CE, Addington J, Goodyear B, Cadenhead KS, Mirzakhanian H, Cornblatt BA, Carrion R, Mathalon DH, McGlashan TH, Perkins DO, Belger A, Seidman L, Thermenos HW, Tsuang MT, van Erp TGM, Walker EF, Hamann S, Anticevic A, Woods SW, Cannon TD. (2018). Cerebello-thalamo-cortical hyperconnectivity: a state-independent neural signature for psychosis prediction and characterization. Nature Communications, 9(1), 3836.

Forsyth, J. K., Lewis, D. A. (2017). Mapping the consequences of impaired synaptic plasticity in schizophrenia through development: An integrative model for diverse clinical features. Trends in Cognitive Sciences, 21(10), 760-778.

Forsyth, J. K., Bachman, P., Mathalon, D. M., Roach, B. J., Ye, E., Asarnow, R. F. (2017). Effects of augmenting N-Methyl-D-Aspartate receptor signaling on working memory and experience-dependent plasticity in schizophrenia: An exploratory study using acute d-cycloserine. Schizophrenia Bulletin, 43(5), 1123-1133.

Schreiner M*, Forsyth JK*, Karlsgodt KH, Anderson AE, Hirsh N, Kushan L, Uddin LQ, Mattiaccio L, Coman IL, Kates WR, Bearden CE. (2017). Intrinsic Connectivity Network-Based Classification and Detection of Psychotic Symptoms in Adolescents and Young Adults with 22q11.2 Deletions. Cerebral Cortex. 27(6):3294-3306. (*co-first author).

Forsyth JK, Ellman LM, Tanskanen A, Mustonen U, Huttunen M, Suvisaari J, Cannon TD. (2013). Genetic risk for schizophrenia, obstetric complications, and adolescent school outcome: Evidence for gene-environment interaction. Schizophrenia Bulletin. 39(5):1067-1076.