As the population is growing older, the risk for dementia increases. The complexity of dementia calls for a multidisciplinary approach; in this project I will combine the research fields of Epidemiology, Genetics, Psychology and Cognitive Neuroscience. It is crucial to identify persons at risk for developing dementia, as possible treatment interventions should be administered in an early stage of disease, before irreversible brain damage has occurred.Recent studies yield evidence that psychosocial stress may play a relevant role in the development of dementia. The exact underlying mechanism between psychosocial stress and dementia is however unclear and therefore I will investigate whether genetic susceptibility and accelerated telomere shortening interact with or mediate the effect of psychosocial stress on the onset of dementia.
First, I propose to investigate whether persons with genetic susceptibilities are more prone for the detrimental effects of psychosocial stress factors on early symptoms of dementia. These genetic susceptibilities will be selected by conducting pathway analysis of mechanisms which have previously been related to dementia.
Second, I will examine whether accelerated telomere shortening can explain the relation between psychosocial stress and early symptoms of dementia. I will do this in two large longitudinal population-based cohort studies, namely the SNAC-K study and SATSA study.
And third I will translate the findings from the epidemiological studies into a cognitive neuroscience experiment in which I will investigate whether the effect of chronic psychosocial stress on brain activity and gray matter volume can be modified by aging and a common genetic variation. This will be done by conducting a functional MRI study using a working memory task and an emotional cognitive control task. This highly innovative and multidisciplinary project will greatly improve our knowledge on how stress affects the aging brain.'