Boris B. Quednow

Boris B. Quednow, Prof. Dr. rer. nat.

zIReN Collaboration Partner

Associate Professor for Experimental and Clinical Pharmacopsychology

Department of Psychiatry Psychotherapy and Psychosomatics UZH


Short bio

Boris B. Quednow studied psychology at the University of Bonn. He wrote his dissertation on the behavioral and neurobiological consequences of “ecstasy” (MDMA) use at the Ruhr-University of Bochum, while working as a research assistant at the Department of Psychiatry of the University of Bonn. At present, he is an Associate Professor of Experimental and Clinical Pharmacopsychology at the Department for Psychiatry, Psychotherapy, and Psychosomatics at the Psychiatric Hospital of the University of Zurich (UZH). He is also affiliated to the Jacobs Center for Productive Youth Development at the UZH, the Psychological Institute of the UZH, the Neuroscience Center Zurich and the Zurich Center for Integrative Human Physiology, both jointly located at the UZH and ETH Zurich, the Competence Center for Mental Health at the UZH, and the Swiss School of Public Health. His main research interests are the behavioral neurotoxicology and neuroplasticity of substance use, the neurochemistry of cognitive functions, behavioral genetics, and disturbed information processing in psychiatric diseases, particularly schizophrenia and drug addiction.

Brief listing of research interests

Behavioral Neurotoxicology, Cognition, Drug-induced Neuroplasticity, Endophenotypes, Neuropsychopharmacology, Substance use and Addiction

Current Projects

The effect of psychosocial and craving-induced stress on social cognition and decision-making in cocaine users: a longitudinal approach
Problematic cocaine use is still a public health issue in Switzerland and across Europe. We have recently shown that cocaine addiction is associated with a variety of social deficits given that affected users showed impaired emotional empathy, behaved less prosocial, experience lower social reward, and reported to have smaller social networks. These social impairments likely contribute to the emergence and maintenance of cocaine addiction and probably hamper psychotherapeutic treatment. Moreover, animal studies and a few cross-sectional studies with cocaine dependent individuals suggest that cocaine use is associated with a increased responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to both stressful social interactions and exposure to cocaine-related cues. It was proposed that the increased susceptibility to stress plays also an important role in the development, preservation, and relapse of cocaine addiction. However, it is not clear yet how psychosocial strain and stress induced by cocaine craving interact with each other and how they specifically impact social cognition and behavior. It is furthermore unclear how alterations of the HPA axis change over time and if they are reversible after prolonged abstinence. Finally, previous research applying laboratory stress to cocaine users exclusively investigated hormonal responses but so far neglected likely changes in the expression of stress-related genes. Therefore, with a longitudinal case-control design we would like to investigate how psychosocial and craving-induced stress responses influence social cognition and social decision-making. Stress responses will be quantified by measurement of stress hormones and expression of HPA-related genes. The longitudinal design additionally allows to explore how physiological stress responses vary with changing cocaine use over time. Finally, we aim to predict the course of objectively determined cocaine misuse by physiological stress-response measures and gene expression patterns.
Longitudinal evaluation of neuroanatomical and behavioral changes associated with altered cocaine consumption
This project investigates changes in brain structures and cognition associated with altered cocaine intake over time. Up to now, it is largely unknown if cognitive deficits and structural brain differences found in cocaine users are in fact induced by drug intake or if they depict a preexistent state. With the application of a longitudinal study design, deeper understanding of the causality between cocaine intake and behavioral/neuroanatomical outcome measures can be gained. Moreover, longitudinal analyses could also help to identify drug-induced neuroplasticity involved in the maintenance of addictive behavior in affected individuals. Such findings are crucial to determine target regions for future psychotherapeutical and pharmacological interventions. With the recollection of data from three already established MR-studies using the identical technical setup, we have the unique opportunity to conduct one of the few longitudinal studies in order to answer several pending questions regarding causality of structural brain abnormalities found in cocaine users previously.
Non-medical prescription opioid use and its neuropsychological and neurobiological predispositions and consequences
Based on increased public health concerns regarding the misuse of opioid analgesics (e.g., morphine, oxycodone, and fentanyl) especially in the U.S. but also in Europe, non-medical prescription opioid use (NMPOU) has become an emerging field in addiction research. The most findings on opioid-related neuropsychological impairments came from studies assessing heroin, buprenorphine, or methadone users. For these populations, it is, however, difficult to attribute their cognitive impairments to the opioid system because of confounding factors such as polydrug use or brain injury caused by overdoses or drug adulterants. Accordingly, the chronic neuropsychological effects of prescription opioid use are scarcely examined to date. Therefore, the present project aims to invetigate chronic effects of NMPOU on neuropsychological, neuroendocrinological, and psychophysiological functions in humans in a longitudinal case-control study design. A specific focus will be on the processing of social pain and empathy for pain, given that a neuronal overlap of physical and social pain (e.g., social rejection, ostracism) has been postulated. During these social neuroscience paradigms endocrinological and electrophysiological stress responses will be assessed.

Selected publications

  • Havranek MM, Vonmoos M, Müller CP, Büetiger JR, Tasiudi E, Hulka LM, Preller KH, Mössner R, Grünblatt E, Seifritz E, Quednow BB (2015). Serotonin transporter and tryptophan hydroxylase gene variations mediate working memory deficits of cocaine users. Neuropsychopharmacology 40: 2929-37
  • Hulka LM, Eisenegger C, Preller KH, Vonmoos M, Jenni D, Bendrick K, Baumgartner MR, Seifritz E, Quednow BB (2014). Altered social and non-social decision-making in recreational and dependent cocaine users. Psychol Med 44: 1015-28.
  • Hulka LM, Treyer V, Scheidegger M, Preller KH, Vonmoos M, Johyem A, Baumgartner MR, Ametamey S, Buck A, Seifritz E, Quednow BB (2014). Smoking but not cocaine use is associated with lower metabotropic glutamate receptor 5 densities in the brain of cocaine users. Mol Psychiatry 19: 625-32.
  • Preller KH, Herdener M, Schilbach L, Stämpfli P, Hulka LM, Vonmoos M, Ingold N, Vogeley K, Tobler PN, Seifritz E, Quednow BB (2014). Functional changes of the reward system underlie blunted response to social gaze in cocaine users. Proc Natl Acad Sci U S A 111: 2842-7.
  • Preller KH, Hulka LM, Vonmoos M, Jenni D, Baumgartner MR, Seifritz E, Dziobek I, Quednow BB (2014). Impaired emotional empathy in cocaine users is related to social network deficits. Addict Biol 19: 452-66.
  • Quednow BB, Brinkmeyer J, Nothnagel M, Mobascher A, Musso F, Gründer G, et al. (2012). Schizophrenia risk polymorphisms in the TCF4 gene interact with smoking in the modulation of auditory sensory gating. Proc Natl Acad Sci U S A 109: 6271-6276.
  • Quednow BB, Treyer V, Hasler F, Dörig N, Wyss MT, Burger C, Rentsch KM, Westera G, Schubiger PA, Buck A, Vollenweider FX (2012). Assessment of serotonin release capacity in the human brain using dexfenfluramine challenge and [18F]altanserin positron emission tomography. NeuroImage 59: 3922-32.
  • Tobler PN, Preller KP, Campbell-Meiklejohn DK, Kirschner M, Krähenmann R, Herdener M, Seifritz E, Quednow BB (2016). Shared neural basis of social and non-social reward deficits in cocaine addiction. Soc Cogn Affect Neurosci 11:1017-25.
  • Vonmoos M, Hulka LM, Preller KH, Minder F, Baumgartner MR, Quednow BB (2014). Cognitive impairment in cocaine users is drug-induced but partially reversible: evidence from a longitudinal study. Neuropsychopharmacology 39: 2200-10.
  • Vonmoos M, Hulka LM, Preller KH, Jenni D, Baumgartner MR, Stohler R, Bolla K, Quednow BB. (2013). Cognitive dysfunctions in recreational and dependent cocaine users: The role of ADHD, craving, and early age of onset. Br J Psychiatry 203: 35-43.

Contact info

Boris B. Quednow, Prof. Dr.
Associate Professor of Experimental and Clinical Pharmacopsychology
Department of Psychiatry, Psychotherapy, and Psychosomatics
Psychiatric Hospital of the University of Zurich
PO Box 1931
Lenggstrasse 31
8032 Zürich / Switzerland
Phone: +41 (0)44 384 27 77
Mail: quednow [at]