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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,
  , 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
  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,
  , 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,
  , 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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• Journal article
  Rintoul J, Butler C, Cleveland R, Grossman Net al., 2026,
  , Nature Communications, Vol: 17, ISSN: 2041-1723

  Non-invasive brain stimulation offers therapeutic potential without surgery, yet existing electrical approaches lack spatial precision due to the long wavelengths of electric fields. Here we demonstrate acoustoelectric neuromodulation, a nonlinear interaction between applied acoustic and electric fields that generates spatially localised, low-frequency electric fields at the ultrasound focus. Using in vitro and in vivo mouse electrophysiology, we show motor-evoked responses that depend on both the amplitude and frequency of the acoustoelectric field, with controls excluding purely acoustic or electrical origins. In vivo measurements show acoustoelectric potentials of ≈9 mV, corresponding to estimated focal electric fields of ~6 V/m at 500 kHz and 1 MPa acoustic pressure, with ~1.5 mm extrema spacing demonstrated in phantom experiments. Importantly, we identify an acoustoelectric contribution to conventional ultrasound stimulation, arising from interactions between ultrasound-induced electrical signals and propagating acoustic waves, establishing acoustoelectric neuromodulation as a distinct mechanism influencing ultrasound-based brain stimulation.

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• Journal article
  Katz DI, Bodien YG, Faerman A, Schwertfeger J, Bogdanova Y, Blum S, Dwyer B, Gilmore N, Goncalves JV, Hays K, Graf MJP, Marino M, Mallas E-J, Shapiro-Rosenbaum A, Sherer M, Williams MW, Zhang Bet al., 2026,
  , J Neurotrauma, Vol: 43, Pages: 835-849

  The post-traumatic confusional state (PTCS) is a period of recovery that follows traumatic brain injury (TBI), characterized by post-traumatic amnesia (PTA), impairments in attention, and behavioral dysregulation, among other clinical symptoms. The pathophysiology of PTCS is unknown, contributing to the absence of neurobiologically based diagnostic criteria, prognostic models, and treatments. The workgroup conducted a scoping review of the literature in MEDLINE/PubMed database and manual searches of references to synthesize the existing knowledge on structural, functional, electroencephalographic (EEG), molecular, and genetic biomarkers underlying PTCS diagnosis and prognosis through five Population, Intervention, Comparison, and Outcome (PICO) questions. The search yielded 3,333 abstracts of which 69 were retained and included. Teams of two workgroup members independently reviewed abstracts and articles. Most articles addressed whether biomarkers differentiated patients with PTCS/PTA from those not in PTCS/PTA, and whether biomarkers were associated with severity or duration of PTCS/PTA. Our findings suggest that transition through PTCS/PTA from lower to higher states of consciousness involves increased thalamic function, restoration of default mode network dynamics, and normalizing of excessive slow wave activity on quantitative EEG. For patients with mild TBI, PTCS/PTA was associated with greater TBI lesion burden on structural imaging. PTCS/PTA severity and duration were associated with lesion burden, reduced white matter integrity, and electrophysiological signatures. Results across studies were variable with many finding no relationship between PTCS/PTA and biomarkers. In summary, while it is premature to include biomarkers in the definition of PTCS/PTA, our findings provide avenues for future research that is designed specifically to address the pathophysiology of this condition.

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