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Sci Rep. 2017 Oct 13;7(1):13187. doi: 10.1038/s41598-017-13282-7.

Psilocybin for treatment-resistant depression: fMRI-measured brain mechanisms.

Author information

1
Psychedelic Research Group, Psychopharmacology Unit, Centre for Psychiatry, Department of Medicine, Imperial College London, W12 0NN, London, UK. r.carhart-harris@imperial.ac.uk.
2
Psychedelic Research Group, Psychopharmacology Unit, Centre for Psychiatry, Department of Medicine, Imperial College London, W12 0NN, London, UK.
3
Computational, Cognitive and Clinical Neuroscience Laboratory (C3NL), Department of Medicine, Imperial College London, W12 0NN, London, UK.
4
Imanova Centre for Imaging Sciences, Burlington Danes Building, Hammersmith Hospital, Du Cane Road, London, W12 0NN, UK.
5
Investigative Medicine, Department of Medicine, Imperial College London, London, United Kingdom.
6
SU/UCT MRC Unit on Risk and Resilience in Mental Disorders, Department of Psychiatry and Mental Health, University of Cape Town, South Africa.
7
Clinical Psychopharmacology Unit, University College London, WC1E 6BT, London, United Kingdom.
8
Cardiff University Brain Research Imaging Centre (CUBRIC), School of Physics and Astronomy, CF24 4HQ, Cardiff, UK.

Abstract

Psilocybin with psychological support is showing promise as a treatment model in psychiatry but its therapeutic mechanisms are poorly understood. Here, cerebral blood flow (CBF) and blood oxygen-level dependent (BOLD) resting-state functional connectivity (RSFC) were measured with functional magnetic resonance imaging (fMRI) before and after treatment with psilocybin (serotonin agonist) for treatment-resistant depression (TRD). Quality pre and post treatment fMRI data were collected from 16 of 19 patients. Decreased depressive symptoms were observed in all 19 patients at 1-week post-treatment and 47% met criteria for response at 5 weeks. Whole-brain analyses revealed post-treatment decreases in CBF in the temporal cortex, including the amygdala. Decreased amygdala CBF correlated with reduced depressive symptoms. Focusing on a priori selected circuitry for RSFC analyses, increased RSFC was observed within the default-mode network (DMN) post-treatment. Increased ventromedial prefrontal cortex-bilateral inferior lateral parietal cortex RSFC was predictive of treatment response at 5-weeks, as was decreased parahippocampal-prefrontal cortex RSFC. These data fill an important knowledge gap regarding the post-treatment brain effects of psilocybin, and are the first in depressed patients. The post-treatment brain changes are different to previously observed acute effects of psilocybin and other 'psychedelics' yet were related to clinical outcomes. A 'reset' therapeutic mechanism is proposed.

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