The Applied Computational Psychiatry lab focuses on developing computational tools with real potential for clinical applications.
Computational Psychiatry is a multidisciplinary field of research at the intersection of psychiatry, neuroscience, machine learning and statistics. The aim of the field is to harness advances in these fields to advance treatments for mental illnesses. For overviews over computational psychiatry, see Huys et al., 2016 Nature Neuroscience and Huys et al. 2020 Neuropsychopharmacology
We are part of the Divison of Psychiatry and the Max Planck UCL Centre for Computational Psychiatry and Ageing Research in the Institute of Neurology at University College London.
When an organ is unable to meet the demands placed on it, illness can arise. As the main functions of the brain are to compute and learn, an understanding of mental illnesses will benefit from an understanding of the computational and learning functions the brain performs, and how these are affected in states of ill-health.
Latest Publications
Cheng, Annie; Konova, Anna; Powers, Albert; Corlett, Philip; Levy, Ifat; Gu, Xiaosi; Huys, Quentin; Pushkarskya, Helen; Fineberg, Sarah; Hauser, Tobias; Bzdok, Danilo; Harpaz-Rotem, Ilan; Babuscio, Theresa; Nichols, Lisa; Zhao, Yize; Sharma, Manu; Meeker, Daniella; Xu, Hua; Rutledge, Robb B.; Pearlson, Godfrey D.; Pittenger, Christopher; Yip, Sarah W.
In: Biological Psychiatry. Cognitive neuroscience and neuroimaging, 2026, ISSN: 2451-9030.
@article{ChengYip26,
title = {Threading the needle: Practical considerations for merging theory-driven computational psychiatry with data-driven analytics to enhance precision health at scale.},
author = {Annie Cheng and Anna Konova and Albert Powers and Philip Corlett and Ifat Levy and Xiaosi Gu and Quentin Huys and Helen Pushkarskya and Sarah Fineberg and Tobias Hauser and Danilo Bzdok and Ilan Harpaz-Rotem and Theresa Babuscio and Lisa Nichols and Yize Zhao and Manu Sharma and Daniella Meeker and Hua Xu and Robb B. Rutledge and Godfrey D. Pearlson and Christopher Pittenger and Sarah W. Yip},
url = {https://acplab.org/wp-content/uploads/publications/ChengYip26.pdf},
doi = {10.1016/j.bpsc.2026.02.009},
issn = {2451-9030},
year = {2026},
date = {2026-02-26},
journal = {Biological Psychiatry. Cognitive neuroscience and neuroimaging},
abstract = {The rapidly evolving field of computational psychiatry enables quantification of specific cognitive processes, and their underlying mechanisms, in a translational and potentially scalable manner, using a combination of data collection via mechanistically informed behavioral tasks and theory-driven mathematical modeling. In parallel, transdiagnostic, dimensional approaches to psychiatric diagnostics, such as RDoC and HiTOP, seek to facilitate links between clinical research and real-world clinical reality, which rarely respects traditional diagnostic boundaries. These two approaches are seldom combined. In addition, while most psychiatric disorders are defined by their longitudinal course, our ability to predict symptom trajectories and tailor treatments to the individual remains limited, in part due to a dearth of longitudinal data collected using assessments sensitive to individual change over time. To address these gaps, the recently launched 'Individually Measured Phenotypes to Advance Computational Translation at Yale' (IMPACT-Y) study is collecting longitudinal data from a transdiagnostic cohort of 2400 individuals, using a combination of 'traditional' clinical research methods (e.g., health records, standardized assessments) and more novel computational approaches (e.g., behavioral tasks with demonstrated sensitivity to latent constructs and to within-person change, spoken narrative data). Here, we discuss unique challenges and opportunities in study design and analysis considerations of IMPACT-Y. Incorporating both theory- and data-driven analytics, we hope that IMPACT-Y will provide an unprecedented resource for characterizing longitudinal trajectories of core computational psychiatry constructs (e.g., reward learning) within and between individuals, for parsing heterogeneity beyond traditional diagnostic categories, and for linking inter- and intra-individual clinical variability to underlying mechanisms.},
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The rapidly evolving field of computational psychiatry enables quantification of specific cognitive processes, and their underlying mechanisms, in a translational and potentially scalable manner, using a combination of data collection via mechanistically informed behavioral tasks and theory-driven mathematical modeling. In parallel, transdiagnostic, dimensional approaches to psychiatric diagnostics, such as RDoC and HiTOP, seek to facilitate links between clinical research and real-world clinical reality, which rarely respects traditional diagnostic boundaries. These two approaches are seldom combined. In addition, while most psychiatric disorders are defined by their longitudinal course, our ability to predict symptom trajectories and tailor treatments to the individual remains limited, in part due to a dearth of longitudinal data collected using assessments sensitive to individual change over time. To address these gaps, the recently launched 'Individually Measured Phenotypes to Advance Computational Translation at Yale' (IMPACT-Y) study is collecting longitudinal data from a transdiagnostic cohort of 2400 individuals, using a combination of 'traditional' clinical research methods (e.g., health records, standardized assessments) and more novel computational approaches (e.g., behavioral tasks with demonstrated sensitivity to latent constructs and to within-person change, spoken narrative data). Here, we discuss unique challenges and opportunities in study design and analysis considerations of IMPACT-Y. Incorporating both theory- and data-driven analytics, we hope that IMPACT-Y will provide an unprecedented resource for characterizing longitudinal trajectories of core computational psychiatry constructs (e.g., reward learning) within and between individuals, for parsing heterogeneity beyond traditional diagnostic categories, and for linking inter- and intra-individual clinical variability to underlying mechanisms.
Fielder, Jennifer C.; Shi, Jinyu; McGlade, Daniel; Huys, Quentin J. M.; Steinbeis, Nikolaus
Sense of control buffers against stress. Journal Article
In: eLife, vol. 14, 2026, ISSN: 2050-084X.
@article{FielderSteinbeis26,
title = {Sense of control buffers against stress.},
author = {Jennifer C. Fielder and Jinyu Shi and Daniel McGlade and Quentin J. M. Huys and Nikolaus Steinbeis},
url = {https://acplab.org/wp-content/uploads/publications/FielderSteinbeis26.pdf},
doi = {10.7554/eLife.105025},
issn = {2050-084X},
year = {2026},
date = {2026-02-26},
journal = {eLife},
volume = {14},
abstract = {Stress is one of the most pervasive causes of mental ill health across the lifespan. Subjective dimensions of stress perception, such as perceived control, are especially potent in shaping stress responses. While the impact of reduced or no control over stress is well understood, much less is known about whether heightened feelings of control buffer against the negative impact of later stress. We designed a novel paradigm with excellent psychometric properties to sensitively capture and induce different states of subjective control. Across two studies with a non-clinical sample of 768 adults, we show a robust association between sense of control and stress as well as symptoms of mental ill health. More importantly, in a subsample of 295 participants, we show that compared to a neutral control group, inducing a heightened state of subjective control buffers against the impact of later stress. These findings demonstrate a causal role for a heightened sense of control in mitigating the negative impact of stressful experiences and spell out important directions for future preventative interventions.},
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Stress is one of the most pervasive causes of mental ill health across the lifespan. Subjective dimensions of stress perception, such as perceived control, are especially potent in shaping stress responses. While the impact of reduced or no control over stress is well understood, much less is known about whether heightened feelings of control buffer against the negative impact of later stress. We designed a novel paradigm with excellent psychometric properties to sensitively capture and induce different states of subjective control. Across two studies with a non-clinical sample of 768 adults, we show a robust association between sense of control and stress as well as symptoms of mental ill health. More importantly, in a subsample of 295 participants, we show that compared to a neutral control group, inducing a heightened state of subjective control buffers against the impact of later stress. These findings demonstrate a causal role for a heightened sense of control in mitigating the negative impact of stressful experiences and spell out important directions for future preventative interventions.
Laszewska, Agata; Helter, Timea; Baldwin, Ashley; Cleare, Anthony J.; Cowen, Philip J.; Evans, Jonathan; Huys, Quentin J. M.; Kurkar, Micheal; Lewis, Alexander C.; Nixon, Neil; Rastogi, Abhinav; Watson, Stuart; Geddes, John R.; Browning, Michael; Simon, Judit
In: The Lancet Regional Health. Europe, vol. 61, pp. 101533, 2026, ISSN: 2666-7762.
@article{LaszewskaSimon26,
title = {Cost-effectiveness of pramipexole augmentation for acute phase and maintenance therapy of treatment-resistant depression compared to placebo augmentation: economic evaluation of the PAX-D randomised controlled trial.},
author = {Agata Laszewska and Timea Helter and Ashley Baldwin and Anthony J. Cleare and Philip J. Cowen and Jonathan Evans and Quentin J. M. Huys and Micheal Kurkar and Alexander C. Lewis and Neil Nixon and Abhinav Rastogi and Stuart Watson and John R. Geddes and Michael Browning and Judit Simon},
url = {https://acplab.org/wp-content/uploads/publications/LaszewskaSimon26.pdf},
doi = {10.1016/j.lanepe.2025.101533},
issn = {2666-7762},
year = {2026},
date = {2026-02-01},
journal = {The Lancet Regional Health. Europe},
volume = {61},
pages = {101533},
abstract = {Pramipexole augmentation of antidepressant treatment for treatment-resistant depression (TRD) has been shown to improve symptom burden over 12 weeks but with some adverse effects compared to placebo augmentation. We aimed to evaluate the cost-effectiveness of pramipexole augmentation for TRD. We conducted an economic evaluation as part of the PAX-D trial over 12 and 48 weeks. Two costing perspectives, National Health Service and Personal Social Services (NHS + PSS) and societal, were adopted. The primary outcome was quality-adjusted life year (QALY) based on the EQ-5D-5L. Secondary outcomes included year of full capability (YFC) based on the ICECAP-A, and capability-weighted life year (CWLY) based on the OxCAP-MH. Incremental cost-effectiveness ratios (ICERs), cost-effectiveness planes and cost-effectiveness acceptability curves were reported alongside sensitivity analyses. The trial was registered with ISCTRN (ISRCTN84666271) and EudraCT (2019-001023-13) and is complete. From the NHS + PSS perspective, mean incremental cost of pramipexole was £60 (95% CI: -£55, £176) over 12 weeks and £811 (95% CI: £110, £1513) over 48 weeks. The difference in QALY gained was 0.012 (95% CI: 0.003, 0.021) over 12 weeks and 0.090 (95% CI: 0.036, 0.144) over 48 weeks, equivalent to 4 (95% CI: 1, 8) and 33 (95% CI: 13, 52) days in perfect health. The ICER was £5069/QALY (95% CI: -£3642, £35,608) over 12 weeks and £9007/QALY (95% CI: £2,219, £27,258) over 48 weeks, representing over 90% probability of cost-effectiveness at £20,000/QALY threshold. From the societal perspective, pramipexole was on average cost saving and more effective over 48 weeks. Alternative analyses provided consistent conclusions. Pramipexole augmentation for TRD has demonstrated both clinical and cost-effectiveness. Further trials, directly comparing pramipexole to other augmentation strategies, will be useful in determining the position of this repurposed medication in the treatment pathway of depression. National Institute for Health and Care Research, Efficacy and Mechanism Evaluation Programme.},
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Pramipexole augmentation of antidepressant treatment for treatment-resistant depression (TRD) has been shown to improve symptom burden over 12 weeks but with some adverse effects compared to placebo augmentation. We aimed to evaluate the cost-effectiveness of pramipexole augmentation for TRD. We conducted an economic evaluation as part of the PAX-D trial over 12 and 48 weeks. Two costing perspectives, National Health Service and Personal Social Services (NHS + PSS) and societal, were adopted. The primary outcome was quality-adjusted life year (QALY) based on the EQ-5D-5L. Secondary outcomes included year of full capability (YFC) based on the ICECAP-A, and capability-weighted life year (CWLY) based on the OxCAP-MH. Incremental cost-effectiveness ratios (ICERs), cost-effectiveness planes and cost-effectiveness acceptability curves were reported alongside sensitivity analyses. The trial was registered with ISCTRN (ISRCTN84666271) and EudraCT (2019-001023-13) and is complete. From the NHS + PSS perspective, mean incremental cost of pramipexole was £60 (95% CI: -£55, £176) over 12 weeks and £811 (95% CI: £110, £1513) over 48 weeks. The difference in QALY gained was 0.012 (95% CI: 0.003, 0.021) over 12 weeks and 0.090 (95% CI: 0.036, 0.144) over 48 weeks, equivalent to 4 (95% CI: 1, 8) and 33 (95% CI: 13, 52) days in perfect health. The ICER was £5069/QALY (95% CI: -£3642, £35,608) over 12 weeks and £9007/QALY (95% CI: £2,219, £27,258) over 48 weeks, representing over 90% probability of cost-effectiveness at £20,000/QALY threshold. From the societal perspective, pramipexole was on average cost saving and more effective over 48 weeks. Alternative analyses provided consistent conclusions. Pramipexole augmentation for TRD has demonstrated both clinical and cost-effectiveness. Further trials, directly comparing pramipexole to other augmentation strategies, will be useful in determining the position of this repurposed medication in the treatment pathway of depression. National Institute for Health and Care Research, Efficacy and Mechanism Evaluation Programme.
Elad, Doron; Story, Giles W.; Berwian, Isabel M.; Stephan, Klaas E.; Walter, Henrik; Huys, Quentin J. M.
Delay discounting correlates with depression but does not predict relapse after antidepressant discontinuation Journal Article
In: Molecular Psychiatry, 2026, ISSN: 1476-5578.
@article{EladHuys26,
title = {Delay discounting correlates with depression but does not predict relapse after antidepressant discontinuation},
author = {Doron Elad and Giles W. Story and Isabel M. Berwian and Klaas E. Stephan and Henrik Walter and Quentin J. M. Huys},
url = {https://acplab.org/wp-content/uploads/publications/EladHuys26.pdf},
doi = {10.1038/s41380-025-03402-5},
issn = {1476-5578},
year = {2026},
date = {2026-01-08},
urldate = {2026-01-08},
journal = {Molecular Psychiatry},
abstract = {Approximately one third of people with Major Depressive Disorder (MDD) experience a relapse within six months of discontinuing antidepressant medication (ADM), however, reliable predictors of relapse following ADM discontinuation are currently lacking. A putative behavioural predictor is delay discounting, which measures a person's impatience to receive reward. Previous studies have linked delay discounting to both MDD and reduced serotonergic function, rendering it a plausible candidate predictor. In this multi-site study we measured delay discounting in participants with remitted MDD (N = 97), before and within six months after discontinuation of ADM, and in matched controls without a lifetime history of MDD (N = 54). Using predictive models, we tested whether either baseline discounting, or an early change in discounting following ADM discontinuation, predicted depressive relapse over a six month follow up period. We also tested differences between remitted MDD and control groups in delay discounting at baseline, and associations between discounting and depressive symptoms. We found that the remitted MDD group, compared to the control group, showed significantly higher (p < 0.05; Cohen's d = 0.34) discounting at baseline. In addition, baseline discounting was positively correlated with depression rating scores (Spearman ρ = 0.24). However, delay discounting did not increase following ADM discontinuation. Neither baseline discounting, nor a change in discounting following ADM discontinuation, predicted subsequent depressive relapse. We conclude that delay discounting is elevated in remitted MDD treated with antidepressant medication. However, delay discounting neither increases following ADM discontinuation, nor does it prospectively predict depressive relapse. These results suggest that delay discounting in Major Depressive Disorder has little relationship with illness trajectory following ADM discontinuation.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Approximately one third of people with Major Depressive Disorder (MDD) experience a relapse within six months of discontinuing antidepressant medication (ADM), however, reliable predictors of relapse following ADM discontinuation are currently lacking. A putative behavioural predictor is delay discounting, which measures a person's impatience to receive reward. Previous studies have linked delay discounting to both MDD and reduced serotonergic function, rendering it a plausible candidate predictor. In this multi-site study we measured delay discounting in participants with remitted MDD (N = 97), before and within six months after discontinuation of ADM, and in matched controls without a lifetime history of MDD (N = 54). Using predictive models, we tested whether either baseline discounting, or an early change in discounting following ADM discontinuation, predicted depressive relapse over a six month follow up period. We also tested differences between remitted MDD and control groups in delay discounting at baseline, and associations between discounting and depressive symptoms. We found that the remitted MDD group, compared to the control group, showed significantly higher (p < 0.05; Cohen's d = 0.34) discounting at baseline. In addition, baseline discounting was positively correlated with depression rating scores (Spearman ρ = 0.24). However, delay discounting did not increase following ADM discontinuation. Neither baseline discounting, nor a change in discounting following ADM discontinuation, predicted subsequent depressive relapse. We conclude that delay discounting is elevated in remitted MDD treated with antidepressant medication. However, delay discounting neither increases following ADM discontinuation, nor does it prospectively predict depressive relapse. These results suggest that delay discounting in Major Depressive Disorder has little relationship with illness trajectory following ADM discontinuation.
Leong, Ian Lam; Ng, Tsz Huen; Sen, Kunal; Burchill, Ella; Costello, Harry; Badenoch, James B.; Coebergh, Jan; McCutcheon, Robert A.; Nair, Akshay; Browning, Michael; Huys, Quentin J. M.; Lewis, Glyn; Lees, Andrew; David, Anthony S.; Rogers, Jonathan P.
Reduced striatal dopamine transmission as a transdiagnostic substrate of psychomotor retardation. Journal Article
In: Brain, 2025, ISSN: 1460-2156.
@article{LeongRogers25,
title = {Reduced striatal dopamine transmission as a transdiagnostic substrate of psychomotor retardation.},
author = {Ian Lam Leong and Tsz Huen Ng and Kunal Sen and Ella Burchill and Harry Costello and James B. Badenoch and Jan Coebergh and Robert A. McCutcheon and Akshay Nair and Michael Browning and Quentin J. M. Huys and Glyn Lewis and Andrew Lees and Anthony S. David and Jonathan P. Rogers},
url = {https://acplab.org/wp-content/uploads/publications/LeongRogers25.pdf},
doi = {10.1093/brain/awaf335},
issn = {1460-2156},
year = {2025},
date = {2025-09-12},
journal = {Brain},
abstract = {Psychomotor retardation, defined as generalised slowing of movement and speech, is a feature of several neurological and psychiatric disorders. In this review, we discuss the hypothesis that reduced striatal dopaminergic transmission is a transdiagnostic substrate for psychomotor retardation underlying the motor features of conditions such as Parkinson's disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia and depression. We examine the evidence across clinical, epidemiological, neuroimaging, laboratory and therapeutic studies. Parkinsonian disorders share slowed movement and a reduction in verbal output with catatonia and depression. Bradyphrenia, slowed cognitive processing, also occurs in Parkinson's disease and depression. In addition, there are close epidemiological relationships between depression and Parkinson's disease, and between catatonia and neuroleptic malignant syndrome. Neuroimaging studies also generally support the association of psychomotor retardation with reduced dopaminergic transmission, particularly in the dorsal striatum. Cerebrospinal fluid measurement of homovanillic acid (a dopamine catabolite) yields inconsistent results and is very nonspecific. Parkinson's disease and catatonia generally respond well to dopaminergic medication. In contrast, dopamine antagonists can induce both parkinsonism and catatonia. Our review is limited by the variability in measurement of psychomotor retardation and difficulty distinguishing between cognitive and motor slowing. It is also likely that other neurotransmitters, such as GABA and serotonin, play an important role in psychomotor speed. It is possible that dopaminergic deficits in psychiatric disorders represent functional disruptions, in contrast to the structural damage to the substantia nigra in Parkinson's disease. We propose further research be conducted into the effects of levodopa and dopamine agonists in depression with psychomotor retardation. Alternative neuroimaging methods such as PET sequences with shorter imaging protocols and neuromelanin-MRI should also be explored.},
keywords = {},
pubstate = {aheadofprint},
tppubtype = {article}
}
Psychomotor retardation, defined as generalised slowing of movement and speech, is a feature of several neurological and psychiatric disorders. In this review, we discuss the hypothesis that reduced striatal dopaminergic transmission is a transdiagnostic substrate for psychomotor retardation underlying the motor features of conditions such as Parkinson's disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia and depression. We examine the evidence across clinical, epidemiological, neuroimaging, laboratory and therapeutic studies. Parkinsonian disorders share slowed movement and a reduction in verbal output with catatonia and depression. Bradyphrenia, slowed cognitive processing, also occurs in Parkinson's disease and depression. In addition, there are close epidemiological relationships between depression and Parkinson's disease, and between catatonia and neuroleptic malignant syndrome. Neuroimaging studies also generally support the association of psychomotor retardation with reduced dopaminergic transmission, particularly in the dorsal striatum. Cerebrospinal fluid measurement of homovanillic acid (a dopamine catabolite) yields inconsistent results and is very nonspecific. Parkinson's disease and catatonia generally respond well to dopaminergic medication. In contrast, dopamine antagonists can induce both parkinsonism and catatonia. Our review is limited by the variability in measurement of psychomotor retardation and difficulty distinguishing between cognitive and motor slowing. It is also likely that other neurotransmitters, such as GABA and serotonin, play an important role in psychomotor speed. It is possible that dopaminergic deficits in psychiatric disorders represent functional disruptions, in contrast to the structural damage to the substantia nigra in Parkinson's disease. We propose further research be conducted into the effects of levodopa and dopamine agonists in depression with psychomotor retardation. Alternative neuroimaging methods such as PET sequences with shorter imaging protocols and neuromelanin-MRI should also be explored.
Latest Preprints
Onysk, Jakub; Chen, Jiazhou; Huys, Quentin JM
On the computational nature of emotions: insights from metareasoning and transformers Journal Article
In: psyArxiv, 2026.
@article{OnyskHuys26,
title = {On the computational nature of emotions: insights from metareasoning and transformers},
author = {Jakub Onysk and Jiazhou Chen and Quentin JM Huys},
url = {https://acplab.org/wp-content/uploads/publications/OnyskHuys26.pdf},
doi = {10.31234/osf.io/m478p_v1},
year = {2026},
date = {2026-05-19},
urldate = {2026-05-18},
journal = {psyArxiv},
publisher = {Center for Open Science},
keywords = {},
pubstate = {published},
tppubtype = {article}
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Serfaty, Jade; Huys, Quentin J. M.
Subjective emotion judgements adhere to principles of Bayesian inference and efficient representation Journal Article
In: psyArxiv, 2026.
@article{SerfatyHuys26,
title = {Subjective emotion judgements adhere to principles of Bayesian inference and efficient representation},
author = {Jade Serfaty and Quentin J. M. Huys},
url = {https://acplab.org/wp-content/uploads/publications/SerfatyHuys26.pdf},
doi = {https://doi.org/10.31234/osf.io/ufmqy_v1},
year = {2026},
date = {2026-05-18},
journal = {psyArxiv},
publisher = {Center for Open Science},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Kim, Taekwan; Viding, Essi; Huys, Quentin J M
Reliable detection of longitudinal change incomputational models Journal Article
In: psyArxiv, 2026.
@article{KimHuys26,
title = {Reliable detection of longitudinal change incomputational models},
author = {Taekwan Kim and Essi Viding and Quentin J M Huys},
url = {https://acplab.org/wp-content/uploads/publications/KimHuys26.pdf},
doi = {https://osf.io/s9dhk},
year = {2026},
date = {2026-04-26},
journal = {psyArxiv},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Hall, Anna F; Huys, Quentin J. M.
Goal progress shapes hedonic experience Journal Article
In: psyArxiv, 2026.
@article{HallHuys26,
title = {Goal progress shapes hedonic experience},
author = {Anna F Hall and Quentin J. M. Huys},
url = {https://acplab.org/wp-content/uploads/publications/HallHuys26.pdf},
doi = {https://doi.org/10.31234/osf.io/4xftg_v1},
year = {2026},
date = {2026-03-11},
journal = {psyArxiv},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bagdades, Elena; Biria, Marjan; Burman, Charlotte; Delpech, Raphaelle; Huys, Quentin J M; Moses-Payne, Madeleine; Norman, Jessica; Pizzagalli, Diego A.; Spencer, Lucienne; Tromans, Naomi; Singh, Ilina; Leigh, Eleanor; Krebs, Georgina; Stringaris, Argyris
Social Surprises and Feedback Shape Momentary Mood and Anxiety in Humans Journal Article
In: PsyArxiv, 2025.
@article{BagdadesStringaris25,
title = {Social Surprises and Feedback Shape Momentary Mood and Anxiety in Humans},
author = {Elena Bagdades and Marjan Biria and Charlotte Burman and Raphaelle Delpech and Quentin J M Huys and Madeleine Moses-Payne and Jessica Norman and Diego A. Pizzagalli and Lucienne Spencer and Naomi Tromans and Ilina Singh and Eleanor Leigh and Georgina Krebs and Argyris Stringaris},
url = {https://acplab.org/wp-content/uploads/publications/BagdadesStringaris25.pdf},
doi = {10.31234/osf.io/a69mz_v2},
year = {2025},
date = {2025-11-05},
journal = {PsyArxiv},
publisher = {Center for Open Science},
keywords = {},
pubstate = {published},
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}