Prof. Peter Brown

Prof. Peter Brown

Director, MRC Programme Leader

Peter Brown is Professor of Experimental Neurology in the Nuffield Department of Clinical Neurosciences, University of Oxford, Honorary Consultant Neurologist at the John Radcliffe Hospital, and Director of the MRC Brain Network Dynamics Unit at the University of Oxford.

After graduating in Medicine at the University of Cambridge, Peter Brown divided his time between the MRC Human Movement and Balance Unit, where he worked as a senior clinical scientist, and the National Hospital for Neurology and Neurosurgery, where he was a Consultant in Neurology. He was appointed a Professor of Neurology at University College London in 2004, and in 2006 he became Head of the Sobell Department of Motor Neuroscience and Movement Disorders at the Institute of Neurology, University College London. He moved to the Nuffield Department of Clinical Neurosciences at the University of Oxford as Professor of Experimental Neurology in 2010. In 2012, he was awarded a Nicholas Kurti Senior Research Fellowship at Brasenose College, Oxford. Professor Brown’s research group has been continuously funded by the Medical Research Council since 1995, and has received additional funding from the European Commission, Wellcome Trust, Rosetrees Trust and National Institute of Health Research Oxford Biomedical Research Centre.

Professor Brown began his research in disorders of Movement in the early 1990s, when he was instrumental in classifying and determining the underlying pathophysiology of myoclonus, and the stiff person and startle syndromes. Later in the 1990s, he developed an interest in the pathophysiology of Parkinson’s disease, which has since been sustained so that he is now one of the leading international figures in the field. Specifically, he has established the importance of exaggerated oscillatory synchronisation in the human disease and demonstrated that the most widely-used animal model of the disease, the 6-hydroxydopamine-lesioned rodent, shares the same pathophysiology. The latter has heightened the value of this model in the investigation of pathological circuit changes and novel treatment approaches. In 2008, he published the first objective demonstration that exaggerated oscillatory activity in the basal ganglia is causally linked to slowness of movement, and that therapeutic deep brain stimulation suppresses such activity.

This interest in Parkinson’s disease has also fuelled studies of healthy subjects where he has shown that more modest degrees of oscillatory synchrony in the motor system facilitate postural activity, whereas oscillations in the higher gamma-frequency band facilitate movement. In 2009, he published the first demonstration that variations in physiological oscillatory activity in the human motor system are causally linked to changes in normal motor behaviour. In 2012, he demonstrated that large behavioural effects could be had from induced oscillatory synchronisation in healthy humans provided that the behavioural context and hence underlying circuit resonances were appropriate.

More recently, Professor Brown’s interests have shifted more towards intervention and therapy. In 2013, he published two seminal proof-of-principle studies implementing adaptive brain-computer interface delivered control at the level of the cortex and of the basal ganglia to control tremor and Parkinsonism in patients. Therapeutic effects were sizeable, and in the case of stimulation of the basal ganglia, surpassed currently available treatment both in terms of efficacy and efficiency. In 2017, he showed that pathological oscillations could be efficiently suppressed by stimulating during certain oscillation phases, with attendant improvements in symptomatic manifestations in the form of tremor. In the same year, his group demonstrated that the pathological beta-band oscillations detected in Parkinson’s disease were markedly bursting in nature and that manipulation of the character of these bursts was a key determinant in the efficacy of levodopa and adaptive deep brain stimulation.