John JB Allen

John JB Allen

Professor, Psychology
Distinguished Professor
Professor, BIO5 Institute
Member of the General Faculty
Professor, Neuroscience - GIDP
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 621-7448

Work Summary

Depression is a major health problem that is often chronic or recurrent. Existing treatments have limited effectiveness, and are provided wihtout a clear indication that they will match a particular patient's needs. In this era of precision medicine, we strive to develop neurally-informed treatments for depression and related disorders.

Research Interest

Dr. Allen’s research spans several areas, but the main focus is the etiology and treatment of mood and anxiety disorders. His work focuses on identifying risk factors for depression using electroencephalographic and autonomic psychophysiological measures, especially EEG asymmetry, resting state fMRI connectivity, and cardiac vagal control. Based on these findings, he is developing novel and neurally-informed treatments for mood and anxiety disorders, including Transcranial Ultrasound, EEG biofeedback, and Transcranial Direct Current and Transcranial Alternating Current stimulation. Other work includes understanding how emotion and emotional disorders influence the way we make decisions and monitor our actions. Keywords: Depression, Neuromodulation, EEG, Resting-state fMRI

Publications

Harmon-Jones, E., & J., J. (1998). Anger and frontal brain activity: EEG asymmetry consistent with approach motivation despite negative affective valence. Journal of Personality and Social Psychology, 74(5), 1310-1316.

PMID: 9599445;Abstract:

The anterior regions of the left and right cerebral hemispheres have been posited to be specialized for expression and experience of approach and withdrawal processes, respectively. Much of the evidence supporting this hypothesis has been obtained by use of the anterior asymmetry in electroencephalographic alpha activity. In most of this research, however, motivational direction has been confounded with affective valence such that, for instance, approach motivation relates positively with positive affect. In the present research, we tested the hypothesis that dispositional anger, an approach-related motivational tendency with negative valence, would be associated with greater left- than right-anterior activity. Results supported the hypothesis, suggesting that the anterior asymmetry varies as a function of motivational direction rather than affective valence. Copyright 1998 by the American Psychological Association, Inc.

Moreno, F. A., Gelenberg, A. J., Heninger, G. R., Potter, R. L., McKnight, K. M., Allen, J., Phillips, A. P., & Delgado, P. L. (1999). Tryptophan depletion and depressive vulnerability. Biological Psychiatry, 46(4), 498-505.

PMID: 10459399;Abstract:

Background: Rapid and transient depletion of tryptophan (TRP) causes a brief depressive relapse in most patients successfully treated with and taking selective serotonin reuptake inhibitors, but little change in drug-free, symptomatic depressed patients. This study investigates the effects of TRP depletion in drug-free subjects in clinical remission from a prior major depressive episode (MDE). Methods: Twelve subjects with a prior MDE, currently in clinical remission and drug-free for at least 3 months (patients), and 12 healthy subjects without personal or family history of Axis I disorder (controls), received TRP depletion. The study was conducted in a double-blind, controlled [full (102-g) and quarter-strength (25 g) 15-amino acid drinks], crossover fashion. Behavioral ratings and plasma TRP levels were obtained prior to, during, and after testing. Results: All subjects experienced significant depletion of plasma TRP on both test-drinks, showing a significant dose-response relation. Healthy control subjects had minimal mood changes, but patients had a depressive response of greater magnitude. Conclusions: In the context of prior TRP depletion studies with antidepressant-treated, and drug-free symptomatic depressed patients, these results suggest that depression may be caused not by an abnormality of 5-HT function, but by dysfunction of other systems or brain regions modulated by 5-HT. Copyright (C) 1999 Society of Biological Psychiatry.

Janssen, C. W., Lowry, C. A., Mehl, M. R., Allen, J. J., Kelly, K. L., Gartner, D. E., Medrano, A., Begay, T. K., Rentscher, K., & White, J. J. (2016). Whole-body hyperthermia for the treatment of major depressive disorder: a randomized clinical trial. JAMA psychiatry, 73(8), 789-795.
Cavanagh, J. F., Zambrano-Vazquez, L., & Allen, J. J. (2012). Theta lingua franca: A common mid-frontal substrate for action monitoring processes. Psychophysiology, 49(2), 220-238.

PMID: 22091878;PMCID: PMC3262926;Abstract:

We present evidence that a multitude of mid-frontal event-related potential (ERP) components partially reflect a common theta band oscillatory process. Specifically, mid-frontal ERP components in the N2 time range and error-related negativity time range are parsimoniously characterized as reflections of theta band activities. Forty participants completed three different tasks with varying stimulus-response demands. Permutation tests were used to identify the dominant time-frequency responses of stimulus- and response-locked conditions as well as the enhanced responses to novelty, conflict, punishment, and error. A dominant theta band feature was found in all conditions, and both ERP component amplitudes and theta power measures were similarly modulated by novelty, conflict, punishment, and error. The findings support the hypothesis that generic and reactive medial prefrontal cortex processes are parsimoniously reflected by theta band activities. © 2011 Society for Psychophysiological Research.

Bismark, A. W., Moreno, F. A., Stewart, J. L., Towers, D. N., Coan, J. A., Oas, J., Erickson, R. P., & Allen, J. J. (2010). Polymorphisms of the HTR1a allele are linked to frontal brain electrical asymmetry. Biological Psychology, 83(2), 153-158.

PMID: 20025927;PMCID: PMC2845287;Abstract:

Polymorphic variations in genes related to serotonin synthesis, transport, recognition, or degradation may convey subtle changes in serotonin system architecture that may place an individual at risk for psychopathology when faced with life stressors. The relationship between three key serotonin alleles and frontal brain electrical asymmetry, a putative endophenotype of depression, was examined. Risk alleles were hypothesized to predict relatively greater right frontal brain activity regardless of current clinical state. A sample of 313 college-age individuals, spanning a range of depressive severity from no symptomotology to clinically meaningful levels, participated. Resting encephalographic (EEG) activity was recorded from 64 scalp sites on four occasions separated by at least 24. h (two 8-min recording sessions occurring at each occasion). Alpha power asymmetry scores between homologous sites were calculated for each session and then averaged to form a trait metric of asymmetry for each pair. PCR based genotyping was conducted for the HTR1a, HTR2a, and HTTLPR genes. Variations in the HTR1a gene were related to trait EEG asymmetry, regardless of any history of depression. Compared to subjects with at least one non-risk allele, subjects with homozygous HTR1A risk alleles had significantly greater relative right frontal activity at sites F7/F8, F5/F6, and F1/F2. In conclusion, variation in HTR1a can influence trait level brain activity, which may ultimately be indicative of risk for psychopathology. © 2009 Elsevier B.V.