The Mach-Gaensslen Foundation of Canada (https://mach-gaensslen.ca/) and JPN have launched an annual award for the best paper published in the journal, to honour the contributions of psychiatrist and former editor Dr. Francis Wayne Quan to the foundation and the journal.
The winners were judged by members of the editorial board who were not authors on JPN research papers. All research papers published in JPN in 2022 were eligible. JPN specifically focuses on papers that provide insights into the neural mechanisms involved in the etiology and treatment of specific psychiatric disorders. Thus, papers were chosen that rated excellent in the following criteria: mechanistic insight, novelty of the findings, innovation of the approach, importance of the contribution, and clarity of the results and conclusions. Because of the number of outstanding candidates, the committee has awarded 3 categories based on the rankings: gold ($2500), silver ($1500) and bronze ($1000).
We are pleased to announce the winners of the prize for 2022. Congratulations!
Gold
Li X, Zhang C, Tan J, Ding L, Wang C, Wang M, Lin Y. Clinical effects of continuous theta burst stimulation for generalized anxiety disorder and a mechanism involving α oscillations: a randomized controlled trial. J Psychiatry Neurosci 2022;47:E123–33. (https://www.jpn.ca/content/47/2/E123).
The use of brain stimulation, while well studied for treatment of depression, has not been studied extensively for treatment of anxiety disorders. Li and colleagues presented the first randomized controlled trial in generalized anxiety disorder comparing 20 sessions of treatment with continuous theta burst stimulation (cTBS), 1 Hz repetitive transcranial magnetic stimulation (rTMS) and sham control over the right dorsolateral prefrontal cortex in a large cohort of 120 patients. They found that anxiety improved in both treatment groups compared with sham stimulation, but that the effect of cTBS but not rTMS persisted at 1 month post-treatment, with more responders and remitters. Furthermore, they were able to begin to address mechanism using resting awake electroencephalography. They found that cTBS produced the greatest increase in α-oscillation frequency, which is related to emotional processing and decreased in anxiety, and correlated with the extent of reduction in anxiety score. These findings are significant in suggesting not only that cTBS may be an optimal method for treating anxiety disorders, but also that post-treatment α-oscillation frequency may provide a useful marker for sustained response to cTBS.
Silver
Cakmak JD, Liu L, Poirier SE, Schaefer B, Poolacherla R, Burhan AM, Sabesan P, St. Lawrence K, Theberge J, Hicks JW, Finger E, Palaniyappan L, Anazodo UC. The functional and structural associations of aberrant microglial activity in major depressive disorder. J Psychiatry Neurosci 2022; 47:E197–208. (https://www.jpn.ca/content/47/3/E197).
Cakmak and colleagues used an innovative hybrid positron emission tomography (PET) and magnetic resonance imaging (MRI) approach to identify a central role for activated microglia in specific brain circuits that correlates with alterations in axonal integrity and functional connectivity, and ultimately with treatment resistance in individuals with major depressive disorder. By linking PET-based changes to diffusion tensor imaging–based and fMRI-based network-level alterations, this work provides a novel approach to understanding at a cellular and molecular level the mechanisms resulting in brain circuitry changes associated with mental illness.
Bronze
Steinmann LA, Dohm K, Goltermann J, Richter M, Enneking V, Lippitz M, Repple J, Mauritz M, Dannlowski U, Opel N. Understanding the neurobiological basis of anhedonia in major depressive disorder — evidence for reduced neural activation during reward and loss processing. J Psychiatry Neurosci 2022;47:E284–92. (https://www.jpn.ca/content/47/4/E284).
In a well-powered study, Steinman and colleagues showed a blunted neural fMRI response to loss, but not reward, in depressed individuals with anhedonia, possibly defining a subphenotype of depression. These changes may be linked with reduced motivation or apathy in patients that contributes to severe anhedonia. This study provides novel mechanistic insights into neural mechanisms underlying anhedonia in individuals with major depressive disorder.
This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is noncommercial (i.e., research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/