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Our group aims to apply computational neuroscience to clinical neurology.

Our integrative approach

We try to break cognition down into its elementary computational steps, asking what quantities the healthy brain must be using
  • Then we try to understand how these steps map on to brain areas and chemicals, e.g. using brain imaging (fMRI, EEG and MEG )
  • Next we study how neurological diseases, such as stroke or dementia, can disrupt cognition. This needs detailed, quantitative characterisation of the clinical problem by studying how patients perform carefully designed tasks.
  • Finally, we ask whether medications can modify cognition. We are particularly interested in the motivational effects of dopamine and acetylcholine.
  • Motivation is what drives us to act. Many diseases alter motivation.

    Damage to some brain areas causes abnormal, misdirected motivation -- sometimes leading to compulsive stereotyped behaviours, or unplanned impulsive acts. This can sometimes be dramatic, causing considerable embarassment for patients and their families.

    A loss of motivation results in clinical apathy -- a disabling disorder that can be difficult to pin down. It is often missed, and is hard to quantify. It carries a huge social and economic burden, and is often frustrating and distressing for carers.

    We study what motivation is, in terms of computations. Is it the selection of an appropriate action, given a goal? Or is it the willingness to invest energy, at a cost, in a rewarding course of action? We found that:

    Working Memory

    Working memory is our ability to hold information in mind, for short periods of time. It can be disrupted by almost any brain problem. It has been difficult to pinpoint where and how such immediate memories are held.

    We study short-term visual memories, measuring our memory capacity, how memories decay, and are disrupted by irrelevant information.