Confirmed speakers

  • Emily Bethell (Liverpool)
  • Lubor Kostal (Bratislava)
  • Susannah Murphy (Oxford)
  • Liz Paul (Bristol)
  • Emma Robinson (Bristol)
  • Rafal Rygula (Krakow)
  • Janna Vrijsen (Nijmegen)
  • Reinout Wiers (Amsterdam)

    Dr Susannah Murphy

    Senior Research Fellow

    Department of Psychiatry

    University of Oxford



    Using experimental models of affective bias to optimise the treatment of depression


    Depression is associated with negative affective biases in information processing, including a tendency to focus on, interpret and remember negative information.  These biases are not only relevant to psychological treatment approaches, but also play a role in pharmacological treatment.  Antidepressants have been shown to reduce negative affective bias using both behavioural and neuroimaging measures of emotional processing in healthy volunteers and depressed patients.  These effects on emotional processing are seen early in antidepressant administration and are predictive of later clinical treatment response, suggesting that early changes in emotional processing can serve as valid surrogate markers of therapeutic efficacy.  In collaboration with pharmaceutical industry, we use these cognitive affective bias measures to screen novel candidate treatments for depression in humans, prior to the initiation of large scale randomised controlled trials.  This experimental medicine approach can be used to assist ‘go/no-go’ decision making in antidepressant drug development, and improve subsequent clinical trial design, dosing and stratification.  

    Emma Robinson, FBPhS

    Professor of psychopharmacology

    School of Physiology, Pharmacology & Neuroscience

    Faculty of Life Sciences

    University of Bristol

    Could modulation of affective biases explain the efficacy of ketamine and other rapid onset antidepressants in major depressive disorder?

    The ability of the NMDA antagonist, ketamine, to induce a rapid reduction in the symptoms of depression, in previously treatment resistant patients, has provided an exciting new avenue for the development of a novel class of antidepressant.  Ketamine has recently been approved by the FDA however there are concerns about side effects and dependence liability meaning alternative compounds are needed.  Current research has focussed on interaction with the processes of synaptogenesis and AMPA modulation, but these studies are limited by the rodent models of depression, which lack translational validity.  In order to try to better understand the underlying mechanisms, which contribute to ketamine’s efficacy, and hence identify novel drug targets, we have been using rodent models of affective bias.  We first showed, in 2015, that acute ketamine could attenuate previously learnt biases in learning and memory.  These effects were localised to the medial prefrontal cortex.  Using a control assay we have also been able to show that these effects are selective to affective bias and do not involve any general effects on memory.  We found similar effects with the muscarinic antagonist scopolamine suggesting that rapid onset antidepressants may share a common mechanism involving modulation of previously acquired negative affective biases.  We have recently extended this work to show that ketamine also has sustained effects and can modulate biases 24hrs after treatment.  In some preliminary studies looking at the molecular mechanisms underlying ketamine’s acute effects, we have found that they do not require protein synthesis but may involve activation of opioid receptors.


    Janna N. Vrijsen, PhD

    Senior researcher

    Department of Psychiatry

    Radboud University Medical Center

    Memory bias modification for depression

    Depression is characterized by negatively biased cognitive processing. Specifically, there is consistent and compelling evidence for the role of negatively biased memory in the etiology of depression. Negative memory bias is most pronounced for self-relevant information e.g. autobiographical events.

    Theory and research on the causal relation between bias and affective symptoms has resulted in the development of Cognitive Bias Modification (CBM) techniques. In depression, CBM has mostly focused on the cognitive domains of attention and interpretation, which so far yielded mixed findings. Modifying memory bias hence seemed promising.

    Our first proof-of-principle studies on CBM-Memory showed that memory bias can be modified and that the training effect transfers to autobiographical memory and mood. A more recent set of two independent trials in depression-vulnerable individuals, however, showed no transfer to depressive symptoms. As a critical test of the clinical applicability of computer-based CBM-Memory, we are currently applying a four-day protocol to depressed


    We recently extended this work by creating a daily-life smartphone-based measure of memory bias, in order to increase validity and facilitating transfer of the training effect. This resulted in. First, we validated this new measure in samples of currently, remitted and never-depressed individuals. As a second step, smartphone-based CBM-Memory was developed and was found to affect autobiographical memory. We are currently exploring its clinical relevance by applying smartphone-based CBM-Memory to a dysphoric (i.e. vulnerable) sample. Smartphone-based memory bias assessment and training may provide a valid extension of the memory bias work so far.


    Reinout Wiers, Ph.D.,

    Professor of developmental psychopathology

    University of Amsterdam

    On the Use of Cognitive Bias Modification in the Treatment of Alcohol Use Disorders

    Alcohol Use Disorders (AUDs) are typically treated with psychosocial treatments and/or medication. However, there is a third category of interventions to consider: varieties of Cognitive Bias Modification (CBM). I will review the current state of affairs. CBM has shown to increase one-year abstinence in several large clinical trials, with effect sizes similar to medication for alcohol (NNT=12). It is also becoming clear for which individuals CBM shows most promise as an add-on treatment (those with a strong cue-reactivity and/or impulsivity), and we are beginning to understand the neurocognitive mechanisms underlying training effects (e.g., reduced cue-reactivity). CBM shows modest but reliable effects as add-on to regular psychosocial treatment, but does not appear to work in the absence of psychosocial treatment, nor in the absence of motivation to change (e.g. in proof-of-principle studies in students). Finally, I will sketch ways forward, such as combining training with neurostimulation.