| Summary: | With the continual growth of the average age of the population and the global rise
in obesity, it is important to investigate age related cognitive decline and its many related
risk factors. Alzheimer’s Disease is the most common cause of dementia and has been
linked to another inflammation-associated disease, atherosclerosis. In our lab’s recent
findings, we have demonstrated this mechanistic link between inflammation and
atherosclerosis with specialized pro-resolving mediators, such as lipoxin and resolvin
found in Omega-3 fatty acids. Here we investigated the viability of our rabbit model of
atherosclerosis as a model of Alzheimer’s Disease, in an effort to eventually test the
impact of inflammation resolution as a treatment to AD. We developed and optimized an
MRI protocol as a way to demonstrate and quantify the effect of vascular inflammation
on a brain ex vivo in first a murine model of arterial stiffness. We then applied the refined
protocol for use on our rabbit model of atherosclerosis. The mouse brains induced with
arterial stiffness showed a significant increase of cerebral microbleeds (indicators of
cerebral amyloid angiopathy). Some of the rabbit brains used for this study were found to
be preserved for too long but found good images in recently harvested and perfused
rabbit brains. While the our findings are currently inconclusive, this thesis proposes a
novel method for investigating the mechanistic and synergistic link between
inflammation, atherosclerosis, and Alzheimer’s Disease.
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