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• Journal article
  Austin B, Kurtin DL, Herlinger K, Hayes A, Hand LJ, Fonville L, Hill RG, Nutt DJ, Lingford-Hughes AR, Paterson LMet al., 2026,

  Investigating hierarchical control among functional networks disrupted by Opioid Use Disorder using effective connectivity

  , Imaging Neuroscience

  <jats:title>Abstract</jats:title> <jats:p>Opioid use disorder (OUD) poses a significant public health challenge. Developing a better understanding of the brain mechanisms and potential markers of OUD would facilitate the development of therapeutic interventions. While we recently showed that between-network connectivity is disrupted in people with OUD compared with healthy controls, it remains unclear what mechanisms may drive these disruptions and how dysfunctional interactions propagate across large scale functional networks. To advance the mechanistic understanding of the disrupted processes in OUD, this study used Effective Connectivity (EC) to quantify disrupted hierarchical control among functional networks governing cognition, attention, and reward. We also explored whether whole-brain patterns of EC were effective markers to distinguish people with severe OUD from controls. We hypothesised that the ventromedial network (VMN) would drive dysfunction in cognitive and attentional networks in people with OUD. Task-fMRI data was collected from healthy controls (HC; n=22) and OUD participants on methadone maintenance treatment (OUD; n=25), during a heroin cue reactivity (CR) and monetary incentive delay (MID) task. Following brain parcellation (214 regions) and network assignment (7 functional networks), EC was quantified using large scale nonlinear Granger causality. Dimensionality reduction was performed using uniform manifold approximation and projection, followed by hierarchical density-based spatial clustering of applications with noise to assess whether EC patterns could form clusters corresponding to group labels.</jats:p> <jats:p>Contrary to our hypothesis, the VMN did not drive dysfunction in cognitive and attentional networks. Instead, edges with significantly stronger EC in HC vs OUD participants were within and between the control, somatomotor, and default mode networks. EC patterns were u

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• Journal article
  Agnorelli C, Peill J, Sawicka G, Kurtin D, Shatalina E, Ahmad K, Wall MB, Rua C, Godfrey K, Ertl N, Searle G, Zhou K, Osugo M, Weiss B, Greenway KT, Fagiolini A, Carhart-Harris R, Matthews PM, Rabiner EA, Nutt D, Erritzoe Det al., 2026,

  Detecting neuroplastic effects induced by ketamine in healthy human subjects: A multimodal approach.

  , J Cereb Blood Flow Metab, Vol: 46, Pages: 2125-2137

  We investigated ketamine's neuroplastic effects in healthy human subjects using integrated Positron Emission Tomography (PET)/Magnetic Resonance Imaging (MRI) measures before and 1-8 days after a single psychedelic dose of ketamine (1 mg/kg, intravenous). Eleven male participants underwent two PET/MRI scans with [11C]-UCBJ (synaptic density/plasticity), 1H-MRS (glutamate and GABA) and resting-state fMRI (intrinsic brain activity, functional connectivity), before and after ketamine. While group-level analyses showed no significant increases in PET synaptic markers, ketamine administration resulted in significantly elevated glutamate levels within the anterior cingulate cortex (ACC). Functional connectivity analyses revealed reduced coupling between the ACC and the dorsolateral prefrontal cortex (dlPFC) and increased coupling between the ACC and the amygdala in the days following ketamine administration. Our multimodal analysis revealed that participants showing an increase in [11C]-UCBJ volume distribution (VT), a putative index of synaptic plasticity, showed a correlated reduction in intrinsic activity within regions belonging to the default mode network (DMN). By linking molecular, cellular and network-level changes, our results point to the DMN as a central hub where ketamine may reshape brain hierarchies in the long term, providing new directions for understanding its therapeutic mechanisms and developing targeted treatments.

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• Journal article
  Bailey NW, Webb SL, Fitzgibbon BM, Denning NC, Dowie T, Schweickle MM, Modak A, Chan G, Knight J, Waldron M, Gainsford K, Hawkes H, Zammit S, Sutanto NC, Godfrey K, Fitzgerald PBet al., 2026,

  No evidence for deleterious effects of psilocybin and MDMA on working memory or related neurophysiological activity in a non-clinical population: An uncontrolled exploratory study.

  , J Psychopharmacol

  BACKGROUND: Research indicates psychedelics hold therapeutic potential, but possible deleterious effects have been insufficiently examined. We explored working memory (WM) performance and WM-related neurophysiological activity before and after exposure to psilocybin or 3,4-methylenedioxymethamphetamine (MDMA) in an uncontrolled study. METHODS: Healthy participants were exposed to a single dose of psilocybin or MDMA (data analysed from 29 participants for each drug, with 16 receiving both drugs after >3-month washout). One to 16 days before and 5-16 days after dosing, participants completed a 3back WM task and eyes-closed resting with electroencephalography (EEG), plus a 3back during a 3-month remote follow-up. RESULTS: After dosing, both groups showed increased alpha to gamma WM-related oscillatory power (p < 0.001). After psilocybin, participants showed steeper WM-related aperiodic slopes (p = 0.018), an effect maximal in occipital electrodes (p < 0.001, Cohen's d = 0.802, BF10 = 155.138), and significant in occipital electrodes during resting (p = 0.008). The MDMA group showed improved task accuracy in the post-dosing EEG session (p = 0.005, Cohen's d = 0.561, BF10 = 7.809). Both groups showed improved accuracy at 3-months (p-holm < 0.001, Cohen's d = 0.678, BF10 = 272.074). CONCLUSIONS: Our results are suggestive of enduring neurophysiological effects following a single dose of MDMA or psilocybin. Our results do not support concerns about cognitive impairments from single exposures to MDMA or psilocybin in controlled settings, suggesting clinical utility does not risk impairing WM. However, given the uncontrolled study design, future research is required to confirm our observations reflect drug-induced neurophysiological changes.

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• Journal article
  Mallas E-J, Moreira da Silva N, Zimmerman KA, Graham NSN, Li LM, David MCB, Busche MA, Taylor PN, Scott G, Sharp DJet al., 2026,

  Brain State Entropy as a Marker of Injury Severity and Sedation Effects Following Traumatic Brain Injury.

  , J Neurotrauma

  Traumatic brain injury disrupts large-scale brain networks. Dynamic functional connectivity captures time-varying network interactions from functional MRI (fMRI) and provides insights into the brain's dynamic patterns of integration and segregation. Here, we investigate dynamic functional connectivity in subacute moderate-severe traumatic brain injury patients (10 days to 6 weeks post-injury) and explore the relationships with blood and imaging biomarkers of injury and propofol sedation. We hypothesized that traumatic brain injury patients would show less complex brain state dynamics that would be associated with greater injury severity measured by white matter integrity and blood biomarkers. Sixty-five subacute traumatic brain injury patients and 48 healthy controls underwent structural and resting-state fMRI. Patients were followed-up at 6 and 12 months post-injury. Plasma concentrations of neurofilament-light chain, microtubule-associated protein, glial fibrillary acidic protein, ubiquitin carboxyl-terminal hydrolase L1, and serum S100 calcium-binding protein B were measured. Fractional anisotropy (FA), a measure of white matter integrity, was derived from diffusion-weighted imaging for a set of white matter tracts. Dynamic functional connectivity analysis was performed using a sliding-window approach. Correlations between time courses of 19 regions of interest representing the default mode network, bilateral frontaloparietal networks, and the salience network were calculated, and k-means clustering was applied to these connectivity matrices. Temporal characteristics of the resulting brain states, including fraction time, dwell time, number of transitions, and entropy of state transitions, were calculated. Four distinct brain states were identified. Brief periods of anticorrelation between key large-scale networks that support cognitive control were a dominant feature. Traumatic brain injury resulted in reduced temporal flexibility, less anticorrelated activity

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• Journal article
  Douglass HM, Spriggs MJ, Godfrey K, Danby JL, de Magalhaes FJC, Macdonald L, Alderton KL, Archer S, Ahmad K, Martell J, Frias JT, Sawicka G, Read T, Blemings A, Lafrance A, Nicholls D, Erritzoe D, Park RJ, Nutt DJ, Carhart-Harris RLet al., 2026,

  Psilocybin therapy for adult females with anorexia nervosa: pilot study.

  , Br J Psychiatry, Pages: 1-9

  BACKGROUND: Anorexia nervosa is a debilitating eating disorder with high mortality and chronicity rates owing to the paucity of effective existing treatments. Several clinical trials using psilocybin therapy have demonstrated therapeutic efficacy and safety in psychiatric conditions, including anorexia nervosa. AIMS: This study aimed to further assess the safety, feasibility and potential efficacy of psilocybin therapy in anorexia nervosa. METHOD: This single-blind, within-individual pilot study recruited 21 females with anorexia nervosa, who underwent three dosing sessions with oral psilocybin (COMP360) over 6 weeks in a fixed order (1 mg, 25 mg, 25 mg), alongside talk therapy and adjunctive to treatment as usual. Adverse events were monitored throughout the study. Primary clinical outcome measures were global Eating Disorder Examination Interview (EDE) and Readiness and Motivation Questionnaire (RMQ) precontemplation scores. Primary time points for the EDE were the 6-week final visit, 3-month follow-up and 6-month follow-up; and for the RMQ, they were the 6-week final visit and comparison between dosing days. Global EDE Questionnaire scores were a key secondary outcome. Key time points were the 6-week final visit and comparison between dosing days. There was a 12-month remote follow-up. RESULTS: Psilocybin was well tolerated by all participants. The most common adverse events were headache, nausea and dizziness. Two serious adverse events (suicide attempts) were reported for one participant within the 6-12-month period. Relative to baseline, participants displayed significant improvements in their eating disorder symptoms (EDE scores: p < 0.0001, d = 0.98, 6 months) and motivation to change (RMQ scores: p = 0.0017, d = 0.65, 12 months). However, there was a large variation in improvement and maintenance during the follow-up. CONCLUSIONS: This study further provides preliminary support for the feasibility, safety and potential efficacy of this intervention to tr

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