Bio

Bio


John obtained his BA in Psychology from UC Berkeley, where he worked in a sleep and psychopathology lab. He then worked in a depression lab at UCSF before entering a PhD program at UCLA, where he conducted research on the relationship between language and thought under the guidance of Dr. Martin Monti. After completing his doctorate in Cognitive Neuroscience, he returned to the Bay Area where he currently is a postdoctoral researcher at the Palo Alto VA in the lab of Dr. Maheen Adamson, where he is developing new treatments for traumatic brain injury, and at Stanford in the Brain Stimulation Lab, where he is developing new treatments for depression. His current focus in both labs is on noninvasive neuromodulation.

Honors & Awards


  • Graduate Student Departmental Fellowship, University of California, Los Angeles, Dept. of Psychology (2011-2012)
  • Graduate Student Research Mentorship, University of California, Los Angeles (2012)

Professional Education


  • Master of Arts, University of California Los Angeles (2013)
  • Doctor of Philosophy, University of California Los Angeles (2018)

Stanford Advisors


Research & Scholarship

Current Research and Scholarly Interests


I am presently engaged in developing innovative treatments for traumatic brain injury in Dr. Maheen Adamson's lab at the Palo Alto VA, and for depression in the Brain Stimulation Lab at Stanford.

Lab Affiliations


Publications

All Publications


  • At the core of reasoning: Dissociating deductive and non-deductive load HUMAN BRAIN MAPPING Coetzee, J. P., Monti, M. M. 2018; 39 (4): 1850–61

    Abstract

    In recent years, neuroimaging methods have been used to investigate how the human mind carries out deductive reasoning. According to some, the neural substrate of language is integral to deductive reasoning. According to others, deductive reasoning is supported by a language-independent distributed network including left frontopolar and frontomedial cortices. However, it has been suggested that activity in these frontal regions might instead reflect non-deductive factors such as working memory load and general cognitive difficulty. To address this issue, 20 healthy volunteers participated in an fMRI experiment in which they evaluated matched simple and complex deductive and non-deductive arguments in a 2 × 2 design. The contrast of complex versus simple deductive trials resulted in a pattern of activation closely matching previous work, including frontopolar and frontomedial "core" areas of deduction as well as other "cognitive support" areas in frontoparietal cortices. Conversely, the contrast of complex and simple non-deductive trials resulted in a pattern of activation that does not include any of the aforementioned "core" areas. Direct comparison of the load effect across deductive and non-deductive trials further supports the view that activity in the regions previously interpreted as "core" to deductive reasoning cannot merely reflect non-deductive load, but instead might reflect processes specific to the deductive calculus. Finally, consistent with previous reports, the classical language areas in left inferior frontal gyrus and posterior temporal cortex do not appear to participate in deductive inference beyond their role in encoding stimuli presented in linguistic format.

    View details for DOI 10.1002/hbm.23979

    View details for Web of Science ID 000427117300030

    View details for PubMedID 29341386

  • Leukocyte telomere length predicts SSRI response in major depressive disorder: A preliminary report. Molecular neuropsychiatry Hough, C. M., Bersani, F. S., Mellon, S. H., Epel, E. S., Reus, V. I., Lindqvist, D., Lin, J., Mahan, L., Rosser, R., Burke, H., Coetzee, J., Nelson, J. C., Blackburn, E. H., Wolkowitz, O. M. 2016; 2 (2): 88–96

    Abstract

    Short leukocyte telomere length (LTL) may be associated with several psychiatric disorders, including major depressive disorder (MDD). Short LTL has previously been associated with poor response to psychiatric medications in bipolar disorder and schizophrenia, but no studies have prospectively assessed the relationship of LTL to SSRI response in MDD. We assessed pre-treatment LTL, depression severity (using the Hamilton Depression Rating Scale [HDRS]), and self-reported positive and negative affect in 27 healthy, unmedicated adults with MDD. Subjects then underwent open-label treatment with a selective serotonin reuptake inhibitor (SSRI) antidepressant for eight weeks, after which clinical ratings were repeated. Analyses were corrected for age, sex and BMI. "Non-responders" to treatment (HDRS improvement <50%) had significantly shorter pre-treatment LTL, compared to "Responders" (p=0.037). Further, shorter pre-treatment LTL was associated with less improvement in negative affect (p<0.010) but not with changes in positive affect (p=0.356). This preliminary study is the first to assess the relationship between LTL and SSRI response in MDD and among the first to prospectively assess its relationship to treatment outcome in any psychiatric illness. Our data suggest that short LTL may serve as a vulnerability index of poorer response to SSRI treatment, but this needs examination in larger samples.

    View details for DOI 10.1159/000446500

    View details for PubMedID 27429957

    View details for PubMedCentralID PMC4943759