Angie Kehagia

My investigations are based on developing paradigms of executive function and decision making as indices of corticostriatal function, sensitive to neuropsychological deficits seen in neurodegenerative conditions and following brain damage. Techniques include fMRI and pharmacology of disease modifying as well as cognitive enhancing drugs, such as levodopa and atomoxetine.

Specifically, my interests lie in noradrenergic dysfunction in Parkinson’s disease, as well as dementia, and developing neuropsychological and neuroimaging methods to improve early and accurate diagnosis with a view to tailoring pharmacotherapy.

In addition to my empirical work in neuroscience, I am interested in philosophical issues surrounding the concept of disorder in the cognitive, affective and psychiatric domains; the social implications of neuroscientific advances; neuroethics.

In 2002, I graduated with a First in Experimental Psychology and was awarded a Newman Exhibition at Balliol College, Oxford.

I subsequently undertook a PhD in Cognitive Neuroscience at Downing College, Cambridge, on a Bill and Melinda Gates scholarship (2003-2007) and a Bursary in Preventive Medicine (2005). My thesis highlighted the heterogeneity of executive dysfunction in Parkinson's disease (PD), aspects of which are dopaminergically insensitive, and proposed a noradrenergic substrate.

My subsequent post-doctoral work at the Behavioural and Clinical Neuroscience Institute at Cambridge was supported by joint MRC/Wellcome Trust funding (2008) and focused on fMRI. As an Isaac Newton Fellow (2009), I ran a novel pharmacological study in PD using the selective noradrenaline reuptake inhibitor atomoxetine to target noradrenergic dysfunction. This double blind randomised placebo controlled study was the first to demonstrate cognitive benefits following the administration of atomoxetine in PD.

I also pursued my growing interest in PD dementia (PDD) in a longitudinal study using fMRI to develop predictive functional biomarkers supported by Parkinson’s UK. In a well-cited review published in Lancet Neurology, and another in Neurodegenerative Diseases, I proposed the Dual Syndrome Hypothesis to explain the distinct evolution of PDD from PD within the broad phenomenology of somatic signs, neuropsychological deficits and neurochemical imbalances.

In addition to my research on the cognitive and psychiatric sequelae of brain damage and neurodegeneration, I undertook a short fellowship in empirical neuroethics at the University of British Columbia in Canada (2010) and managed the International Neuroethics Network.

I returned to the UK as a Research and Teaching Fellow at the University of St Andrews, where I extended my work in task switching to probe the effects of ageing.

I joined King's as a Lecturer in Neuropsychology in 2012, to continue my research in PD with new colleagues at the Deparment of Neuroimaging.