Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom; Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom; Friedman Brain Institute, Fishberg Department of Neuroscience, Icahn School of Medicine, New York, United States
Michael AP Bloomfield
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom; Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom; Division of Psychiatry, University College London, London, United Kingdom; Clinical Psychopharmacology Unit, Research Department of Clinical, Educational and Health Psychology, University College London, London, United Kingdom
Mattia Veronese
Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Jasmin Kroll
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Vyacheslav R Karolis
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Sameer Jauhar
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom; Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom
Ilaria Bonoldi
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom; Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom
Philip K McGuire
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Shitij Kapur
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Robin M Murray
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom
Chiara Nosarti
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King's College London, London, United Kingdom
Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's Health Partners, King's College London, London, United Kingdom; MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom; Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom
Perinatal brain injuries, including hippocampal lesions, cause lasting changes in dopamine function in rodents, but it is not known if this occurs in humans. We compared adults who were born very preterm with perinatal brain injury to those born very preterm without perinatal brain injury, and age-matched controls born at full term using [18F]-DOPA PET and structural MRI. Dopamine synthesis capacity was reduced in the perinatal brain injury group relative to those without brain injury (Cohen’s d = 1.36, p=0.02) and the control group (Cohen’s d = 1.07, p=0.01). Hippocampal volume was reduced in the perinatal brain injury group relative to controls (Cohen’s d = 1.17, p=0.01) and was positively correlated with striatal dopamine synthesis capacity (r = 0.344, p=0.03). This is the first evidence in humans linking neonatal hippocampal injury to adult dopamine dysfunction, and provides a potential mechanism linking early life risk factors to adult mental illness.
