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The influence of functional connectivity on cognitive reserve

Chef d'équipe 
  • Jonathan Epp, University of Calgary
  • Azrieli Foundation

Aperçu du projet

Declining cognitive activity is associated with a wide-variety of neurodegenerative disorders, brain injuries as well as with normal aging despite any clear pathological condition. With normal aging, there is a diverse spectrum of cognitive decline with some individuals showing strong impairments while others show very little loss in cognitive ability. In the case of brain damage or disease, there is also a range of cognitive symptoms that may occur. A possible explanation for the disparity in cognitive decline would be that it relates to the degree of damage in the brain. Although there is typically an association between the amount of pathological damage and the severity of cognitive symptoms it is not the case that individuals with similar pathology will have similar cognitive impairments.

These observations have led to the identification of a phenomenon known as cognitive reserve. Cognitive reserve simply means that some individuals appear to be more resistant to cognitive decline in the face of brain injury or disease. It has been observed in several conditions that individuals with more cognitive activity, higher education, or enriching life experiences are likely to have higher cognitive reserve. However, the mechanisms that result in this neuroprotective effect are not understood. We will develop a mouse model of cognitive reserve based on daily cognitive stimulation to study the morphological and network level changes that are induced by cognitive activity. We will then apply this approach to a mouse model of Alzheimer’s disease to test whether cognitive activity can slow or prevent the onset of cognitive decline and brain pathology.

We anticipate that our findings will generate an improved understanding of the mechanism of cognitive decline, cognitive reserve and memory storage in general. In addition, we expect to develop a greater understanding of neuroprotective mechanisms.