Masud Husain
British professor and editor
From Wikipedia, the free encyclopedia
Masud Husain FRS FRCP FMedSci[2] is a clinical neurologist and neuroscientist at the University of Oxford.[3][1] He is Professor of Neurology & Cognitive Neuroscience at the Nuffield Department of Clinical Neurosciences[4] and Departmental of Experimental Psychology,[5] University of Oxford, a Professorial Fellow at New College, Oxford,[6] and Editor-in-Chief of the journal Brain.[7][8] Husain's book Our Brains, Our Selves won the Royal Society Trivedi Best Science Book Prize, 2025.[9] He was born in East Pakistan, now Bangladesh.[citation needed]
Masud Husain | |
|---|---|
Husain in 2023 | |
| Born | Masud Husain |
| Education | King Edward VI Camp Hill School for Boys |
| Alma mater | University of Oxford (BMBCh, DPhil) |
| Awards | Harkness Fellowship Wellcome Trust Principal Research Fellowship (2012) |
| Scientific career | |
| Fields | Cognitive neurology Working memory Apathy Alzheimer's disease Parkinson's disease[1] |
| Institutions | |
| Thesis | On hemispheric specialisation and visual direction sense (1987) |
| Website | www |
Education
Husain was educated at King Edward VI Camp Hill School for Boys, Birmingham, and studied medicine at the University of Oxford where he was a student at New College, Oxford and received a Bachelor of Medicine, Bachelor of Surgery (BMBCh) degree[5] followed by a DPhil in 1987.[10]
Research and career
Husain held a Harkness Fellowship as a postdoctoral fellow in the laboratory of Richard A. Andersen at Massachusetts Institute of Technology (MIT).[11] He completed his clinical and neurological training at hospitals in Oxford and London.[4]
Husain's research focuses on cognitive functions in people with neurological diseases and healthy people.[4][5][12][13][14][15][16][17][18]
In an editorial in 2025, Husain criticised the rise of bullshit jobs in Universities in the United Kingdom.[7]
Attention and inattention
His work on people with hemispatial neglect following stroke demonstrated several novel components of this syndrome. Using the attentional blink paradigm he showed that there were non-spatial, selective attention deficits in these patients,[19] in addition to their well-established directional attentional bias. Subsequent behavioural studies revealed that some people with hemispatial neglect can also suffer from impaired spatial working memory,[20] often revisiting locations without being aware that they have fixated them before.[21][22] Some may have poor sustained attention as measured on vigilance tasks,[23] or even directional motor deficits as indexed by paradigms where the spatial location of a visual target is dissociated from direction of movement required to reach it.[24][25] These findings provided further evidence for neglect being a multi-component syndrome, with different patients having different deficits, depending upon the extent of their lesion.[26][27] Critical brain regions associated with neglect that were identified by this work, included the right inferior posterior parietal and frontal regions.[28][29] Experimental medicine studies by Husain's group using the dopamine agonist rotigotine[30] and the noradrenergic agonist guanfacine[31][32] demonstrated that these drugs can ameliorate hemispatial neglect to some extent by improving attention.
Visual short-term or working memory
By using new methods to measure the precision of recall in healthy people, work in Husain's lab challenged the view that capacity of visual short-term memory or working memory is limited to a fixed number of items.[33][34] Instead, this research revealed that although short-term memory is a highly limited resource, it can be flexibly deployed depending upon task demands.[35] This work led to the application of new methods to measure short-term memory in patients with Alzheimer's disease,[36][37] Parkinson's disease[36][37][38] and individuals at risk of developing these conditions.[36][37][38][39] The techniques that have been developed can provide more sensitive ways to measure short-term memory than traditional methods.[40] They have also revealed how different mechanisms might underlie short-term memory disorders in different neurological conditions.[37]
Motivation, apathy and initiation of action
Work from Husain's lab showed that lesions to ventral basal ganglia leads to a condition of profound apathy, manifest as a lack of motivation to initiate action and specifically attributable to a deficit in reward sensitivity.[41] Using the dopamine receptor agonist ropinirole, it was possible to improve reward sensitivity, restore motivational vigour and reverse apathy.[41] These observations stimulated larger-scale studies in Parkinson's disease, a condition associated with basal ganglia pathology and often debilitating apathy. The syndrome of pathological apathy in Parkinson's disease[42][43] and small vessel cerebrovascular disease[44][45] was found to be characterised by reduced sensitivity to rewards, a deficit that could be ameliorated by dopaminergic drugs in Parkinson's disease.[42][43] This has led to a theoretical framework to understand mechanisms underlying apathy across brain disorders which incorporates concepts from cost-benefit decision making to formalise how people differ in their willingness to engage in effort in order to obtain potential rewards.[46]
The basal ganglia are considered to be essential for linking motivation to action systems.[47] Outputs of the basal ganglia are strongly connected to medial frontal cortex. Husain's group identified a mechanism that resolves competition between conflicting action plans, in medial frontal brain regions, including the supplementary eye field,[48] supplementary motor area and pre-supplementary motor area.[49][50] A key component of voluntary control paradoxically appears to involve inhibition of unwanted actions that are primed automatically by seeing objects around us.[51] This control is lost following supplementary motor area and pre-supplementary motor area lesions. Findings from lesion, stimulation and physiological studies were incorporated to provide a new theoretical framework for the role of the supplementary motor area and pre-supplementary motor area complex.[52]
Awards and honours
Husain held a Wellcome Trust Senior Research Fellowship at Imperial College London (2000-2007) and University College London (UCL) (2007–12). He was awarded a Wellcome Trust Principal Research Fellowship (2012-2023) and elected Fellow of the Academy of Medical Sciences (FMedSci) in 2008.[2] Husain was awarded the Graham Bull Prize in Clinical Science by the Royal College of Physicians in 2006, British Neuropsychological Society's Elizabeth Warrington Prize (2006),[53] and the European Academy of Neurology Investigator Award (2016).[54] He is Fellow of the American Academy of Neurology (2018) and Fellow of the European Academy of Neurology (2018),[55] and is co-lead of the National Institute for Health and Care Research (NIHR) Oxford Health Biomedical Research Centre Dementia theme (2022 -)[56] and Dementia Research Oxford at the University of Oxford.[57] He was elected a Fellow of the Royal Society in 2026.[58]