Emotional and cognitive changes during neuroinflammation

It is now increasingly recognized that anxiety and cognition symptoms in MS are primary effects of the disease, rather than psychological consequences of living with a chronic illness. To date, only a limited number of investigations of the molecular basis of these symptoms, based on the EAE model, have been conducted. These studies concluded that hitherto unknown pathological mechanisms underlie these defects.

Our preliminary data, on the other hand, support classical immunopathological processes as the basis of anxiety and cognition problems in EAE. In collaboration with Dr Matthew Hale, Department of Psychology and Counselling, LTU, we have begun investigations of the timing of onset and severity of these deficits in EAE, using well established behavioural approaches including the elevated plus maze and novel object recognition tests. Data will be correlated with cellular and molecular changes in the relevant brain regions, namely the hippocampal formation and striatum. For these investigations we will use the MOG35-55–induced NOD/Lt and C57Bl/6 variants and the PLP180-199-induced BALB/c variant.  Additionally the capacity of MS drugs, for example FTY720 (aka Fingolimod or Gilenya), to ameliorate these symptoms will be examined. We will also compare responses between EAE variants on disease development and severity and drug treatment.