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As Professor of Cognitive Neurology James studies the mechanisms and treatment of frontotemporal dementias, Progressive Supranuclear Palsy, corticobasal syndrome and related disorders. These are united in their high rates of apathy and impulsivity, and pressing need for better treatments. James trained in medical sciences and experimental psychology at Cambridge, before clinical training in Oxford and his PhD at UCL, London. After specialist training in London and Copenhagen, he returned to Cambridge where he now leads the Dementia theme of the NIHR Biomedical Research Centre, and directs the Cambridge Centre for Frontotemporal Dementia. He is Associate Director of Dementias Platform UK, and Chief Scientific Adviser to Alzheimer’s Research UK. His work brings together deep- phenotyping, brain imaging, genetics, computational modelling, pharmacology and cognitive neuroscience to understand the mechanisms of disease and individual differences, as the pathway to new treatments. He is an active clinical neurologist, which underlies his determination that research focusses on the priorities for people affected by frontotemporal dementia.Apathy and Impulsivity are common and disabling features of many neurological and psychiatric disorders. They are associated with worse prognosis and higher carer burden and costs. It has been common to attribute them to hypo- and hyper-dopaminergic states respectively, affecting motivation though changes in reward sensitivity or effort avoidance. However, there are problems with this prevailing dogma. First, apathy and impulsivity are positively correlated in health and many diseases (ie. more apathetic people are also more impulsive), inconsistent with simplistic concepts of hypo- versus hyper-dopaminergic states. Second, dopaminergic therapies have been largely ineffective in treating apathy. Here we re-consider apathy and impulsivity, bringing together epidemiological evidence, structural and functional brain imaging, psychopharmacology and insights from the translation of cognitive neuroscience paradigms to clinical populations. These lead to an alternative framework for apathy and impulsivity, seen jointly as a failure of behavioural decision making.We introduce a novel Bayesian brain approach, in which apathy arises not from actions being undesirable or effortful, but from their being unnecessary to achieve ones goals – or more exactly, to be close enough to ones goals in the absence of behaviour. And we the review evidence of the importance of noradrenergic regulation of behaviour, which is leading to more effective therapies for apathy and impulsivity. Finally, we consider the need for better tools to quantify apathy and impulsivity, appropriate for specific clinical populations. The evidence base draws mainly on Parkinson’s disease, Alzheimer’s disease and disorders associated with frontotemporal lobar degeneration, but is relevant to people affected by the wide range of disorders studied and managed by members of the BNPA.