J.F.W. Deakin

The University of Manchester, Manchester, England, United Kingdom

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Publications (206)1105.92 Total impact

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    ABSTRACT: Objectives Immune mechanisms have been implicated in the pathogenesis of schizophrenia. This has lead to clinical trials of re-purposing drugs with off-target anti-inflammatory actions. They include the antibiotic minocycline and simvastatin (HMP-Co reductase inhibitor), which decrease microglial activation, and ondansetron a 5-HT3-receptor antagonist that has limited effects on cytokine production. This presentation will address their efficacy and mechanism of action. Aims 1) Update on trials with minocycline including our own positive finding on negative symptoms (PMID: 16959472) 2) Present new results with ondansetron and simvastatin summarised below. Methods Ondansetron (8mg) and simvastatin (40mg) vs placebos in 2×2 design (PMID: 23782463). Patients aged 18-65, stable treatment, DSM IV schizophrenia-related diagnosis. PANSS and cognition at 0,3,6 months. Results The four cells of the 2×2 design contained 302 patients. The interaction between ondansetron and simvastatin was significant at p=.006 reflecting the lower scores in the 3 active treatment groups than in the P+P group. Ondansetron improved verbal (p=.007) and visual list learning (p=.02) with no other treatment effects on cognition. Conclusions Minocycline appears to benefit negative symptoms in early psychosis with a minor effect on cognition. Simvastatin had limited effects in our patients with established schizophrenia but its anti-inflammatory effects could be worth investigating in early psychosis. Ondansetron has a significant effect on new learning, which might be expected from its 5-HT3 antagonist properties. This may underlie a benefit on negative symptoms reported by others and us.
    23 European Congress of Psychiatry,, Vienna, Austria,; 03/2015
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    R Zahn · K E Lythe · J.A. Gethin · S Green · J F W Deakin · C Workman · J Moll ·
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    ABSTRACT: One influential view is that vulnerability to major depressive disorder (MDD) is associated with a proneness to experience negative emotions in general. In contrast, blame attribution theories emphasise the importance of blaming oneself rather than others for negative events. Our previous exploratory study provided support for the attributional hypothesis that patients with remitted MDD show no overall bias towards negative emotions, but a selective bias towards emotions entailing self-blame relative to emotions that entail blaming others. More specifically, we found a decreased proneness for contempt/disgust towards others relative to oneself (i.e. self-contempt bias). Here, we report a definitive test of the competing general negative versus specific attributional bias theories of MDD. We compared a medication-free remitted MDD (n=101) and a control group (n=70) with no family or personal history of MDD on a previously validated experimental test of moral emotions. The task measures proneness to specific emotions associated with different types of self-blame (guilt, shame, self-contempt/disgust, self-indignation/anger) and blame of others (other-indignation/anger, other-contempt/disgust) whilst controlling for the intensity of unpleasantness. We confirmed the hypothesis that patients with MDD exhibit an increased self-contempt bias with a reduction in contempt/disgust towards others. Furthermore, they also showed a decreased proneness for indignation/anger towards others. This corroborates the prediction that vulnerability to MDD is associated with an imbalance of specific self- and other-blaming emotions rather than a general increase in negative emotions. This has important implications for neurocognitive models and calls for novel focussed interventions to rebalance blame in MDD. Copyright © 2015. Published by Elsevier Masson SAS.
    European Psychiatry 03/2015; 30(4). DOI:10.1016/j.eurpsy.2015.02.005 · 3.44 Impact Factor
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    European Psychiatry 03/2015; 30. DOI:10.1016/S0924-9338(15)30060-2 · 3.44 Impact Factor
  • I. Koychev · A. Shepherd · W. El-Deredy · J.F.W. Deakin · C. Haenschel ·

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    ABSTRACT: Background: Prosocial emotions related to self-blame are important in guiding human altruistic decisions. These emotions are elevated in major depressive disorder (MDD), such that MDD has been associated with guilt-driven pathological hyper-altruism. However, the impact of such emotional impairments in MDD on different types of social decision-making is unknown. Method: In order to address this issue, we investigated different kinds of altruistic behaviour (interpersonal cooperation and fund allocation, altruistic punishment and charitable donation) in 33 healthy subjects, 35 patients in full remission (unmedicated) and 24 currently depressed patients (11 on medication) using behavioural-economical paradigms. Results: We show a significant main effect of clinical status on altruistic decisions (p = 0.04) and a significant interaction between clinical status and type of altruistic decisions (p = 0.03). More specifically, symptomatic patients defected significantly more in the Prisoner's Dilemma game (p < 0.05) and made significantly lower charitable donations, whether or not these incurred a personal cost (p < 0.05 and p < 0.01, respectively). Currently depressed patients also reported significantly higher guilt elicited by receiving unfair financial offers in the Ultimatum Game (p < 0.05). Conclusions: Currently depressed individuals were less altruistic in both a charitable donation and an interpersonal cooperation task. Taken together, our results challenge the guilt-driven pathological hyper-altruism hypothesis in depression. There were also differences in both current and remitted patients in the relationship between altruistic behaviour and pathological self-blaming, suggesting an important role for these emotions in moral and social decision-making abnormalities in depression.
    Psychological Medicine 10/2014; 45(06):1-13. DOI:10.1017/S0033291714002414 · 5.94 Impact Factor
  • A. Dutta · S. McKie · J.F.W. Deakin ·

  • C.S. Symonds · C.C. Henson · J.F.W. Deakin · I.M. Anderson ·

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    ABSTRACT: Major depressive disorder (MDD) is associated with abnormalities in financial reward processing. Previous research suggests that patients with MDD show reduced sensitivity to frequency of financial rewards. However, there is a lack of conclusive evidence from studies investigating the evaluation of financial rewards over time, an important aspect of reward processing that influences the way people plan long-term investments. Beck's cognitive model posits that patients with MDD hold a negative view of the future that may influence the amount of resources patients are willing to invest into their future selves. We administered a delay discounting task to 82 participants: 29 healthy controls, 29 unmedicated participants with fully remitted MDD (rMDD) and 24 participants with current MDD (11 on medication). Patients with current MDD, relative to remitted patients and healthy subjects, discounted large-sized future rewards at a significantly higher rate and were insensitive to changes in reward size from medium to large. There was a main effect of clinical group on discounting rates for large-sized rewards, and discounting rates for large-sized rewards correlated with severity of depressive symptoms, particularly hopelessness. Higher discounting of delayed rewards in MDD seems to be state dependent and may be a reflection of depressive symptoms, specifically hopelessness. Discounting distant rewards at a higher rate means that patients are more likely to choose immediate financial options. Such impairments related to long-term investment planning may be important for understanding value-based decision making in MDD, and contribute to ongoing functional impairment.
    Psychological Medicine 11/2013; 44(9):1-10. DOI:10.1017/S0033291713002584 · 5.94 Impact Factor
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    D Arnone · S McKie · R Elliott · G Juhasz · E J Thomas · D Downey · S Williams · J F W Deakin · I M Anderson ·
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    ABSTRACT: Reduced hippocampal volume has been reported in depression and may be involved in the aetiology of depressive symptoms and vulnerability to depressive relapse. Neuroplasticity following antidepressant drug treatment in the hippocampus has been demonstrated in animal models but adaptive changes after such treatment have not been shown in humans. In this study, we determined whether grey matter loss in the hippocampus in depression (1) is present in medication-free depressed (2) changes in response to antidepressant treatment and (3) is present as a stable trait in medication-free remitted patients. Sixty-four medication-free unipolar depressed patients: 39 currently depressed and 25 in remission, and 66 healthy controls (HC) underwent structural magnetic resonance imaging in a cross-sectional and longitudinal design. Thirty-two currently depressed participants were then treated with the antidepressant citalopram for 8 weeks. Adherence to treatment was evaluated by measuring plasma citalopram concentration. We measured regional variation in grey matter concentration by using voxel-based morphometry-Diffeomorphic Anatomical Registration Through Exponentiated Lie algebra. Patients with current depression had bilaterally reduced grey matter in the hippocampus compared with HC and untreated patients in stable remission with the latter groups not differing. An increase in grey matter was observed in the hippocampus following treatment with citalopram in currently depressed patients. Grey matter reduction in the hippocampus appears specific to the depressed state and is a potential biomarker for a depressive episode.Molecular Psychiatry advance online publication, 6 November 2012; doi:10.1038/mp.2012.150.
    Molecular Psychiatry 11/2012; 18(12). DOI:10.1038/mp.2012.150 · 14.50 Impact Factor
  • J.F.W. Deakin · D. Hodkinson · J. Gigg · S.R. Williams ·

    European Neuropsychopharmacology 10/2012; 22:S135. DOI:10.1016/S0924-977X(12)70171-2 · 4.37 Impact Factor
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    I Koychev · W El-Deredy · T Mukherjee · C Haenschel · J F W Deakin ·
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    ABSTRACT: Core symptoms of schizophrenia, particularly in the cognitive domain are hypothesized to be due to an abnormality in neural connectivity. Biomarkers of connectivity may therefore be a promising tool in exploring the aetiology of schizophrenia. We used electrophysiological methods to demonstrate abnormal visual information processing during in patients performing a simple cognitive task. Electrophysiological recordings were acquired from 20 chronically ill, medicated patients diagnosed with either schizophrenia or schizo-affective disorder and 20 healthy volunteers while they conducted a working memory (WM) task. The patient group had significantly lower accuracy on the WM task and a trend for slower responses. An early visual evoked response potential was reduced in patients. Analysis of the electroencephalographic oscillations showed a decreased phase-locking factor (in the theta, beta and gamma bands) and signal power (theta frequency band). The beta and gamma oscillatory abnormalities were confined to two sets of correlated fronto and occipital electrodes. The findings of event-related potential and oscillatory abnormalities in patients with schizophrenia confirm the sensitivity of early visual information processing measurements for identification of schizophrenia phenotype. The fronto-occipital distribution of the oscillatory abnormalities replicates our findings from a schizotypal sample and implicates a possible top-down dysfunction as a vulnerability trait.
    Acta Psychiatrica Scandinavica 03/2012; 126(1):59-71. DOI:10.1111/j.1600-0447.2012.01849.x · 5.61 Impact Factor

  • 24th Congress Meeting of European-College-of-Neuropsychopharmacology24th Congress Meeting of European-College-of-Neuropsychopharmacology; 09/2011
  • C. S. Symonds · S. McKie · R. Elliott · J. F. W. Deakin · I. M. Anderson ·

    European Neuropsychopharmacology 09/2011; 21. DOI:10.1016/S0924-977X(11)70512-0 · 4.37 Impact Factor
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    M E Palm · R Elliott · S McKie · J F W Deakin · I M Anderson ·
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    ABSTRACT: Generalized anxiety disorder (GAD) is under-researched despite its high prevalence and large impact on the healthcare system. There is a paucity of functional magnetic resonance imaging (fMRI) studies that explore the neural correlates of emotional processing in GAD. The present study investigated the blood oxygen level dependent (BOLD) response to processing positive and negative facial emotions in patients with GAD. A total of 15 female GAD patients and 16 female controls undertook an implicit face emotion task during fMRI scanning. They also performed a face emotion recognition task outside the scanner. The only behavioural difference observed in GAD patients was less accurate detection of sad facial expressions compared with control participants. However, GAD patients showed an attenuated BOLD signal in the prefrontal cortex to fearful, sad, angry and happy facial expressions and an attenuated signal in the anterior cingulate cortex to happy and fearful facial expressions. No differences were found in amygdala response. In contrast with previous research, this study found BOLD signal attenuation in the ventrolateral and medial prefrontal cortex and the anterior cingulate cortex during face emotion processing, consistent with a hypothesis of hypo-responsivity to external emotional stimuli in GAD. These decreases were in areas that have been implicated in emotion and cognition and may reflect an altered balance between internally and externally directed attentional processes.
    Psychological Medicine 05/2011; 41(5):1009-18. DOI:10.1017/S0033291710001455 · 5.94 Impact Factor

  • European Neuropsychopharmacology 03/2011; 21. DOI:10.1016/S0924-977X(11)70099-2 · 4.37 Impact Factor
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    E J Thomas · R Elliott · S McKie · D Arnone · D Downey · G Juhasz · J F W Deakin · I M Anderson ·
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    ABSTRACT: Both past depressive episodes and the personality trait of depressive rumination are strong risk factors for future depression. Depression is associated with abnormal emotional processing, which may be a neurobiological marker for vulnerability to depression. A consistent picture has yet to emerge as to how a history of depression and the tendency to ruminate influence emotional processing. The aim of this study was to investigate the relationship between rumination, past depression and neural responses when processing face emotions. The Ruminative Responses Scale (RRS) was completed by 30 remitted depressives and 37 controls who underwent functional magnetic resonance imaging (fMRI) scanning while viewing happy, sad, fearful and neutral faces. The remitted depressives showed overall reductions in neural responses to negative emotions relative to the controls. However, in the remitted depressives, but not the controls, RRS scores were correlated with increased neural responses to negative emotions and decreased responses to happiness in limbic regions. Automatic emotion processing biases and rumination seem to be correlated to aspects of vulnerability to depression. However, remission from depression may be maintained by a general suppression of limbic responsiveness to negative emotion.
    Psychological Medicine 02/2011; 41(9):1845-55. DOI:10.1017/S0033291711000043 · 5.94 Impact Factor
  • J F W Deakin · J Harro · I M Anderson ·

    European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 01/2011; 21(1):1-2. DOI:10.1016/j.euroneuro.2010.11.008 · 4.37 Impact Factor
  • J. Lazary · G. Juhasz · I. Anderson · J. F. Deakin · G. Bagdy ·

    European Psychiatry 12/2010; 25:1437-1437. DOI:10.1016/S0924-9338(10)71421-8 · 3.44 Impact Factor
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    ABSTRACT: Lesions of the orbital prefrontal cortex (OPFC) and the nucleus accumbens core (AcbC) can disrupt performance in inter-temporal choice tasks, possibly by increasing the organism's sensitivity to delay and/or magnitude of reinforcement. This experiment examined whether exposure to an inter-temporal choice would induce neuronal activation in these areas, as indicated by enhanced expression of the Fos protein. Twelve rats were trained to press levers A and B under an adjusting-delay schedule in which a response on A delivered 50 microl of a sucrose reinforcer after 2 or 18s, whereas a response on B delivered the same reinforcer after a delay that was adjusted in accordance with the rat's choices. Another 12 rats were trained under a similar schedule in which a response on A delivered an immediate reinforcer of size 20 or 180 microl, whereas a response on B delivered an immediate reinforcer whose size was adjusted in accordance with the rat's choices. A third group received training under a schedule that did not entail variation of reinforcer size or delay, or choice between reinforcers, and a control group underwent food restriction without behavioural training. Exposure to the adjusting-delay schedule was associated with enhanced Fos expression in both the OPFC and AcbC, whereas exposure to the adjusting-magnitude schedule was associated with enhanced Fos expression in the OPFC but not the AcbC, compared to the control group. The results are consistent with previous findings that implicated the AcbC and OPFC in delay discounting, and the OPFC in sensitivity to reinforcer size.
    Behavioural brain research 12/2010; 213(2):269-77. DOI:10.1016/j.bbr.2010.05.014 · 3.03 Impact Factor

Publication Stats

8k Citations
1,105.92 Total Impact Points


  • 1985-2014
    • The University of Manchester
      • Neuroscience & Psychiatry Unit
      Manchester, England, United Kingdom
    • MRC Clinical Sciences Centre
      London Borough of Harrow, England, United Kingdom
  • 2008
    • University of Melbourne
      • Department of Psychiatry
      Melbourne, Victoria, Australia
  • 2001
    • Imperial College London
      • MRC Clinical Sciences Centre
      Londinium, England, United Kingdom
    • University of Oxford
      • Department of Psychiatry
      Oxford, England, United Kingdom
  • 1999
    • University of Cambridge
      Cambridge, England, United Kingdom
  • 1996
    • Advance MRI
      Frisco, Texas, United States
  • 1993
    • University of Bristol
      Bristol, England, United Kingdom
  • 1990
    • University Hospital Of South Manchester NHS Foundation Trust
      Manchester, England, United Kingdom
  • 1976-1981
    • MRC National Institute for Medical Research
      • Division of Neurophysiology
      Londinium, England, United Kingdom
  • 1975
    • Florida Clinical Research Center
      Florida, United States